NEUROSURGERY

CRANIO-CEREBRAL INJURIES

(Head Injuries – Part 1)

I. Introduction and Epidemiology

Head injuries are a frequent cause of emergency admissions. Each year, approximately 300 out of 100,000 people are
hospitalized due to head trauma. About 9 per 100,000 die as a result — equating to roughly 5,000 deaths annually in the UK.
Some deaths are inevitable due to the nature of the injury, but others may be preventable with proper management.

Common causes include:

• Road traffic accidents (most common and severe, especially in young males)
• Falls
• Assaults
• Injuries during sports or at home/work

Contributing factors:

• Alcohol consumption (especially in road accidents)

• Lack of protective measures (e.g. seatbelts, helmets)

Goal of management:
Since primary brain damage cannot be reversed once sustained, treatment focuses on preventing or minimizing secondary
complications (e.g., hypoxia, swelling, infection, hematoma).

II. Pathological Classification

Head injuries are classified into:

A. By Nature of Damage

1. Focal – localized injuries such as contusions or hematomas

2. Diffuse – widespread injury like axonal shearing

B. By Timing

1. Primary injury – happens at the moment of trauma (impact)

2. Secondary injury – occurs afterward due to complications (e.g., swelling, ischemia, infection)

III. Focal Injuries

1. Cortical Contusions and Lacerations

• May occur under the site of impact or opposite to it (contre-coup injuries)

• Frontal and temporal lobes are most commonly affected
• Usually multiple and bilateral
• By themselves, they don’t cause unconsciousness — but bleeding into contusions can form hematomas which do
2. Intracranial Hematomas

Divided by location and type:

Type Description
Extradural Blood collects outside the dura, usually due to torn middle meningeal vessels (often from skull fractures
(epidural) in the temporal area)
Intradural Includes:Subdural hematoma – rupture of bridging veins between cortex and dural sinuses; Intracerebral
hematoma – bleeding into brain parenchyma; These may coexist or appear as a burst lobe
Combination May occur simultaneously (e.g., subdural + intracerebral)

⚠ Note: A hematoma may result in brain compression, midline shift, or herniation.

3. Tentorial and Tonsillar Herniation

• Due to rising intracranial pressure (ICP)

• Sequence:
o Midline shift
o Lateral tentorial herniation (medial temporal lobe compresses midbrain)
o Central tentorial herniation
o Tonsillar herniation (cerebellar tonsils herniate through foramen magnum, compressing brainstem)
• May cause rapid deterioration and brainstem death

4. Infective Complications

• Occur with compound fractures, dural tears, or basal skull fractures

• Lead to:
o Meningitis
o Cerebral abscess

IV. Diffuse Injuries

1. Diffuse Axonal Injury (DAI)

• Caused by shearing forces during sudden acceleration/deceleration

• Axons are stretched/torn, especially at:
o Corpus callosum
o Pons
o Superior cerebellar peduncle
• Cellular damage worsens over 48 hours due to:
o Excitotoxic neurotransmitters
o Calcium influx
o Phospholipid cascade
o Possibly genetic risk (APOE ε4 gene)
• Results range from mild coma to death

Microscopic findings:

• Retraction balls (damaged axons)

• Microglial clusters (inflammatory response)

2. Cerebral Ischemia

• Caused by hypoxia or impaired perfusion

• After trauma, autoregulation may fail → hypotension leads to decreased cerebral perfusion pressure (CPP) → worsens
neuronal damage
• Contributing factors: glutamate toxicity, free radicals
3. Cerebral Swelling (Edema)

• Due to vascular congestion or fluid accumulation

• Pathology may not be visible macroscopically but may show:
o Hemorrhagic tears (esp. corpus callosum, cerebellar peduncles)
o Seen after survival of several days to weeks
• Wallerian degeneration may appear after 5 weeks

Next Part (Part 2) will include:

• Clinical Assessment (e.g., consciousness levels, signs of basal skull fracture)

• Investigations (CT, X-ray, monitoring ICP)
• Management strategies (resuscitation, transfer, surgery)
• Complications (chronic subdural hematoma, meningitis)

CRANIO-CEREBRAL INJURIES

(Head Injuries – Part 2: Clinical Assessment and Diagnostic Features)

Initial Clinical Assessment of Head Injury

The evaluation of a patient with a head injury must begin with a careful and structured approach, recognizing that life-
threatening complications can be both neurological and systemic. Clinical signs may not always correlate immediately with the
extent of brain injury; therefore, assessment must be both repeated and thorough.

1. Consciousness Level

The most important initial observation is the level of consciousness, which is best quantified using the Glasgow Coma Scale
(GCS). This scale, developed in Glasgow in 1974, assesses three core responses:

• Eye opening
• Verbal response
• Motor response

These categories are scored individually. Although the total GCS score provides an overview, the most accurate practice is to
record each component separately, rather than summing the score.

• For example, a patient who opens eyes only to pain, speaks in confused sentences, and localizes to pain would be
described as:
E2 V4 M5 rather than a score of "11".

Changes in the GCS are critical for monitoring neurological deterioration, especially in the first hours after injury.

2. Signs Suggestive of Specific Types of Brain Injury

Lucid Interval

In some cases, notably extradural hematoma, the patient may lose consciousness at the time of impact, then regain awareness
(lucid interval) before deteriorating again due to rising intracranial pressure from hematoma expansion. This classic pattern is
rare, but must be recognized promptly.
Base of Skull Fracture

Certain clinical signs point toward a fracture at the base of the skull, which has diagnostic and prognostic importance. These
include:

• Periorbital bruising ("raccoon eyes") – suggests anterior fossa fracture

• Bruising over the mastoid process (Battle’s sign) – indicates middle cranial fossa fracture
• Clear fluid (CSF) rhinorrhoea or otorrhoea – strongly indicates dural tear with CSF leak
• Hemotympanum (blood behind the tympanic membrane)

If CSF leak is suspected, testing of the fluid can reveal glucose or beta-2 transferrin, which are indicative of cerebrospinal fluid.

3. Neurological Deficits

Although many patients with mild injuries do not exhibit clear focal neurological signs, in moderate to severe cases the presence
of asymmetrical pupil response, motor deficits, or abnormal posturing (e.g., decerebrate or decorticate rigidity) are key
features that demand urgent attention.

• Unilateral dilated pupil may signal compression of the third cranial nerve due to uncal herniation
• Hemiparesis or extensor posturing in response to pain is indicative of brainstem dysfunction
• Seizures immediately after trauma may occur in cortical contusions or penetrating injuries

4. Late Deterioration

Some patients deteriorate hours after the injury, despite initially mild symptoms. Causes include:

• Expanding intracranial hematoma (epidural or subdural)

• Cerebral edema
• Seizures
• Hypoxia or hypotension (exacerbating secondary brain injury)

This highlights the importance of continued monitoring, especially in patients with:

• GCS less than 15

• Neurological signs
• Skull fracture
• Vomiting
• Seizures

These cases should be observed in a clinical setting for at least 24 hours, even if initial CT is normal.

5. Post-Traumatic Amnesia (PTA)

This refers to the time from the injury until the patient regains continuous memory. It is an important measure of injury
severity.

• Short PTA (<1 hour): minor injury

• PTA of 1–24 hours: moderate
• PTA >24 hours: severe

Assessment of PTA helps in prognostication and rehabilitation planning.

6. Indications for Urgent Investigation and Neurosurgical Referral

Some key clinical signs that should prompt immediate CT scanning and referral to neurosurgical unit include:

• GCS <13 at any point

• GCS <15 for more than 2 hours
• Suspected open or depressed skull fracture
• Any sign of basal skull fracture
• More than one episode of vomiting
• Seizure(s) post-injury
• Focal neurological deficit
• Age >65 with head injury
• Bleeding tendency or on anticoagulant therapy (e.g. warfarin)

7. CT Scan Findings

CT scan is the gold standard for evaluating acute head injuries.

The scan may reveal:

• Extradural hematoma – typically biconvex (lens-shaped), sharply demarcated

• Subdural hematoma – crescent-shaped, may cross suture lines
• Cerebral contusion – patchy low density with possible petechial hemorrhages
• Midline shift – indicates mass effect
• Ventricular compression or hydrocephalus
• Basal cistern obliteration – may indicate herniation or raised intracranial pressure
• Skull fractures – linear or depressed

In cases of suspected CSF leak, or penetrating injury, thin-slice CT of the skull base or 3D reconstructions may be useful.

8. Skull X-ray

Although now largely replaced by CT, a skull X-ray may still have a role in specific settings, such as identifying:

• Depressed fractures
• Foreign bodies
• Surgical planning
• Fractures involving paranasal sinuses or orbit

However, its diagnostic value is limited, and it is generally not relied upon for definitive assessment.

Next, in Part 3, I will continue with:

• Management strategies (prehospital care, airway, resuscitation)

• Neurosurgical interventions
• Monitoring intracranial pressure (ICP)
• Management of raised ICP
• Prevention of complications
• Outcome and prognostic factors
• Chronic subdural hematoma
CRANIO-CEREBRAL INJURIES

(Head Injuries – Part 3: Management, Surgery, and Intracranial Pressure)

Initial Management Principles

The clinical priority in any patient with a head injury is to identify and treat life-threatening conditions promptly, especially
when the patient has impaired consciousness. In the acute setting, the initial medical goal is not necessarily to diagnose the full
extent of intracranial damage, but to ensure systemic stability and prevent secondary brain injury.

The key elements of early management include:

• Airway protection
• Adequate oxygenation
• Maintaining cerebral perfusion
• Avoiding further hypoxia or hypotension
• Monitoring for signs of neurological deterioration

Even patients who appear stable initially can deteriorate over time due to expanding hematomas, brain swelling, or seizures.
Therefore, vigilance and repeated assessments are vital.

Airway, Breathing, Circulation (ABC)

In an unconscious or semiconscious patient, the airway may be obstructed by the tongue, blood, vomit, or facial fractures.
Immediate steps must be taken to clear and secure the airway, often requiring:

• Oropharyngeal suction
• Head positioning with neck stabilization
• Endotracheal intubation in patients with a GCS <9, or those unable to protect their airway

Once the airway is secure, attention is directed to ventilation and oxygenation. Adequate oxygen delivery is essential to prevent
hypoxic brain damage, especially when cerebral autoregulation is impaired.

Circulatory support follows. Hypotension, even for a short period, significantly worsens brain injury outcomes. If systolic blood
pressure falls below 90 mmHg, urgent volume replacement (crystalloids or blood) is necessary to restore cerebral perfusion
pressure.

Spinal Injury Consideration

Until spinal injury is excluded by imaging, the cervical spine must be immobilized using a hard collar or appropriate manual
stabilization. This is crucial in polytrauma cases, where spinal fractures may be masked by unconsciousness or distracting
injuries.

Indications for Hospital Transfer

Any patient who:

• Remains unconscious or confused

 • Has focal neurological signs
• Demonstrates signs of raised intracranial pressure
• Has evidence of skull fracture
• Experiences seizures
• Has co-existing systemic injuries

should be transferred to a neurosurgical center for definitive assessment and management. It is important that transfer is not
delayed by waiting for local investigations, such as imaging, if these would not influence the immediate management or alter
the need for referral.

Neurosurgical Assessment and Emergency Surgery

The role of the neurosurgeon in head injury management is centered around timely identification of lesions that may benefit
from surgical intervention. In particular, expanding hematomas (such as epidural or subdural collections), penetrating injuries,
and cases of depressed skull fractures may require urgent operative decompression.

Surgical Indications Include:

• Evidence of mass effect with midline shift

• Significant intracranial hematoma with neurological deterioration
• Compound depressed skull fractures
• Persistent CSF leakage
• Penetrating cranial injuries

A craniotomy is typically performed to evacuate hematomas or repair dural tears. In certain cases, burr holes may be used as a
temporary decompression measure while awaiting definitive care.

Intracranial Pressure (ICP) Monitoring

For patients with a severe head injury (GCS ≤8), or evidence of intracranial mass effect on CT, intracranial pressure monitoring
is recommended. This helps to guide therapy aimed at preventing further cerebral ischemia.

ICP can be measured using:

• Intraventricular catheter (allows both monitoring and CSF drainage)

• Intraparenchymal fiber-optic transducer
• Subdural or epidural sensors (less accurate, used when ventricles are inaccessible)

Normal ICP in adults is typically 5–15 mmHg. An ICP greater than 20 mmHg, especially when sustained, is associated with poorer
outcomes and requires intervention.

Management of Raised Intracranial Pressure

When raised ICP is suspected or confirmed, a stepwise approach to management is adopted:

1. Basic Measures:
o Elevation of the head to 30 degrees to promote venous drainage
o Optimizing oxygenation and avoiding hypercapnia
o Maintaining adequate blood pressure to ensure cerebral perfusion
o Sedation and analgesia to reduce cerebral metabolic demand
2. Hyperosmolar Therapy:
o Mannitol (0.25–1 g/kg IV) or hypertonic saline may be administered to reduce cerebral edema
o Repeated dosing must be carefully balanced to avoid hypotension and renal impairment
3. Controlled Ventilation:
 o Hyperventilation can lower PaCO₂, causing cerebral vasoconstriction and ICP reduction, but should be used
cautiously and for short durations, as prolonged hypocapnia may cause cerebral ischemia
4. Surgical Decompression:
o If ICP remains unresponsive, decompressive craniectomy may be required
o Hematoma evacuation or CSF drainage via ventriculostomy may also be considered
5. Barbiturate Coma:
o In refractory cases, barbiturate-induced coma may reduce cerebral metabolic demand and ICP, though it
carries significant risks

Seizure Prophylaxis and Management

Seizures can occur either:

• Immediately after injury (within 24 hours), or

• Late after days to weeks

Although prophylactic antiepileptic drugs (e.g., phenytoin or levetiracetam) may reduce the incidence of early post-traumatic
seizures, there is no evidence that they prevent the development of post-traumatic epilepsy.

Therefore, seizure prophylaxis is often reserved for:

• Penetrating injuries
• Cortical contusions
• Depressed skull fractures
• Subdural hematomas
• Severe brain swelling

Once a seizure occurs, treatment is initiated using intravenous benzodiazepines, followed by maintenance with standard
antiepileptics.

Infection Control and CSF Leak

Patients with compound skull fractures or dural tears are at risk of meningitis. CSF rhinorrhoea or otorrhoea must be treated
with:

• Prophylactic antibiotics in some cases (though this remains controversial)

• Surgical repair if leakage persists beyond several days or if meningitis develops
• Avoidance of nasal instrumentation or nasogastric tubes in patients with known anterior fossa fractures

In Part 4, I will continue with:

• Post-traumatic complications (e.g., chronic subdural hematoma, delayed hematomas)

• Long-term effects and rehabilitation
• Outcome determinants
• Brain death criteria and ethical considerations after traumatic brain injury
CRANIO-CEREBRAL INJURIES

(Head Injuries – Part 4: Delayed Effects, Chronic Subdural Hematoma, and Outcome)

Delayed Effects of Head Injury

Even after initial stabilization and early recovery, some patients exhibit delayed complications that may not have been apparent
in the acute phase. These can manifest days, weeks, or even months after the original injury. These effects are especially likely in
elderly patients, those with cortical atrophy, or in individuals receiving anticoagulation therapy.

One of the most clinically significant delayed consequences is the chronic subdural hematoma, though other long-term
sequelae such as post-traumatic epilepsy, cognitive impairment, and personality change are also recognized.

Chronic Subdural Hematoma

A chronic subdural hematoma develops due to persistent or slow venous bleeding, usually from ruptured bridging veins
between the brain's surface and the dural sinuses. The condition evolves over weeks, often following minor trauma, which the
patient may not even recall. It is more common in:

• Elderly patients, due to cerebral atrophy that stretches the veins

• Patients on anticoagulant therapy
• Those with alcoholism, epilepsy, or coagulopathy

In these individuals, even trivial trauma can cause bleeding that accumulates slowly in the subdural space. Over time, this
hematoma becomes encapsulated by membranes, with repeated microhemorrhages and breakdown of blood products
contributing to osmotic expansion of the collection.

Because the hematoma is slowly expanding, there is often no dramatic loss of consciousness. Instead, patients typically present
with progressive neurological deterioration, which may mimic other cerebral pathologies such as stroke or dementia.

Clinical Features of Chronic Subdural Hematoma

The presentation is insidious. Patients may initially appear normal after injury, only to develop gradually worsening symptoms
over days or weeks. The clinical signs depend on the location, size, and rate of expansion of the hematoma. Common
manifestations include:

• Headache, often dull and generalized, worsening over time

• Drowsiness, confusion, or personality change
• Slowing of mental function, memory disturbance
• Focal neurological deficits, such as:
o Hemiparesis
o Dysphasia
o Gait disturbance
o Visual field deficits
• Seizures may also occur

In some cases, the presentation mimics Parkinson’s disease, depression, or even dementia, especially in elderly patients.
Therefore, a high index of suspicion is necessary.
Diagnosis of Chronic Subdural Hematoma

The diagnosis is usually confirmed with neuroimaging, and the modality of choice is CT scan. The appearance of a chronic
subdural hematoma on CT differs from acute subdural hemorrhage in several ways:

• It typically appears as a hypodense (dark) or isodense crescent-shaped area overlying the cerebral hemisphere.
• In some cases, mixed-density or multilayered appearances occur due to rebleeding.
• Mass effect may be evident, such as compression of the lateral ventricle or midline shift.
• In certain chronic cases, the hematoma may become bilateral, further complicating the clinical picture.

When CT scan is inconclusive, or to better delineate the membranes or identify isodense collections, MRI may provide superior
sensitivity.

Management of Chronic Subdural Hematoma

Treatment is usually surgical, and the goal is to evacuate the hematoma, relieve mass effect, and prevent recurrence. The most
common surgical approach is burr hole drainage, often performed under local or general anesthesia. The procedure includes:

• One or two burr holes made over the affected hemisphere

• Opening of the dura and outer membrane
• Irrigation of the hematoma cavity with saline
• Placement of a closed drainage system, typically left for 24–48 hours

In some recurrent or thick-membraned cases, craniotomy may be required to remove the outer and inner membranes, though
this is less common.

Following surgery, the patient's neurological status is closely monitored, and repeat imaging is often performed to confirm
resolution.

In frail patients or those unfit for surgery, a conservative approach may be considered, especially if the hematoma is small and
asymptomatic, though close follow-up is essential.

Outcome After Brain Injury

The prognosis after a head injury varies significantly depending on multiple factors:

• Severity of the initial insult (as measured by GCS)

• Presence of intracranial mass lesions
• Patient age
• Time to treatment
• Occurrence of secondary insults such as hypoxia, hypotension, or seizures

Patients with mild head injuries generally recover completely, although post-concussion symptoms such as headache, dizziness,
and irritability may persist for several weeks.

In moderate to severe injuries, recovery is more variable. Some patients regain full function, while others may suffer:

• Persistent cognitive impairment

• Personality changes
• Emotional lability
• Chronic fatigue
• Focal neurological deficits
Neuropsychological assessment often reveals subtle impairments even when imaging appears normal. These may affect return
to work or academic performance.

In the most severe cases, especially with prolonged coma, diffuse axonal injury, or bilateral uncal herniation, the outcome may
be persistent vegetative state or death.

Rehabilitation is essential and should begin as early as feasible. It includes:

• Physical therapy
• Cognitive and occupational therapy
• Psychological support
• Family education and reintegration programs

Brain Death Following Severe Head Injury

In certain cases of massive brain injury, the damage is so extensive that brainstem function is irreversibly lost. This condition is
termed brain death and is considered equivalent to death in most legal and medical systems.

Diagnosis of brain death is strictly clinical and must be performed according to national protocols. The essential criteria include:

• Deep unresponsive coma of known cause

• Absence of brainstem reflexes, including:
o Pupillary light reflex
o Corneal reflexes
o Gag and cough reflexes
o Vestibulo-ocular response (caloric testing)
• No spontaneous respiration, confirmed by apnea test
• Exclusion of reversible causes, such as hypothermia, drug intoxication, or metabolic disturbance

Two experienced physicians must independently confirm the findings. Ancillary tests such as EEG or cerebral angiography may
be used when clinical examination is equivocal.

In confirmed cases, organ donation may be discussed with the family, as many patients who progress to brain death are
otherwise young and previously healthy.

In the next section, Part 5, I will cover:

• Post-traumatic epilepsy
• Post-concussion syndrome
• Long-term neuropsychological effects
• Neurorehabilitation strategies and outcomes
CRANIO-CEREBRAL INJURIES

(Head Injuries – Part 5: Post-Traumatic Epilepsy, Post-Concussion Syndrome, Neurocognitive Sequelae, and Rehabilitation)

Post-Traumatic Epilepsy (PTE)

Following a head injury, seizures may occur at different stages, and the risk of developing epilepsy is directly correlated with the
severity and type of injury. Post-traumatic seizures are categorized by timing:

• Immediate seizures: occurring within the first 24 hours post-injury

• Early seizures: occurring within 1 week of injury
• Late seizures: developing after more than 1 week post-injury — these are considered true post-traumatic epilepsy

The incidence of post-traumatic epilepsy is highest in cases involving:

• Penetrating brain injury

• Depressed skull fractures
• Cortical contusions or lacerations
• Intracerebral hematomas
• Prolonged coma or dural tears

The risk of developing epilepsy increases with longer durations of unconsciousness, presence of early seizures, and younger age
at the time of injury.

Prophylactic anticonvulsant therapy may be considered to reduce the incidence of early seizures, particularly within the first 7
days, although evidence suggests this does not reduce the long-term risk of epilepsy. Medications like phenytoin,
carbamazepine, or levetiracetam are commonly used.

Once epilepsy is established, long-term anticonvulsant treatment is initiated, tailored to seizure type and EEG findings. Some
patients may eventually achieve seizure freedom and discontinue medication after a sustained seizure-free period (usually over
2 years), depending on the risk profile.

Post-Concussion Syndrome (PCS)

Post-concussion syndrome refers to a set of symptoms that persist for weeks or months following a mild head injury, typically
with no structural lesion seen on imaging. This syndrome is particularly frequent after:

• Acceleration–deceleration injuries (e.g., road traffic accidents)

• Mild closed head injuries with transient loss of consciousness or even without loss of consciousness

Symptoms typically include:

• Persistent headache
• Fatigue
• Dizziness or light-headedness
• Irritability or emotional lability
• Poor concentration
• Insomnia
• Memory difficulties
• Depression or anxiety

These symptoms often cause significant distress and functional impairment, especially in occupational or academic settings.
The underlying mechanisms remain poorly understood. Functional imaging may show hypometabolism in the frontal lobes, but
standard CT or MRI scans are usually normal. There may be a contribution from subtle axonal injury, neurochemical imbalance,
and psychological response to trauma.

Management is supportive and based on a multidisciplinary approach:

• Reassurance and education about the benign nature of the condition

• Analgesia for headache, avoiding medication overuse
• Cognitive behavioral therapy for emotional or psychological distress
• Occupational therapy to facilitate return to work or study
• Gradual return to activity, avoiding both overstimulation and prolonged inactivity

In most cases, post-concussion syndrome gradually resolves within three to six months, but in a minority, symptoms may persist
longer.

Neuropsychological and Behavioral Consequences

Severe head injuries frequently result in lasting cognitive and personality changes, even in the absence of major motor deficits.
These changes may not be obvious on physical examination but can profoundly affect the patient’s ability to reintegrate into
society.

Cognitive deficits may include:

• Reduced attention span

• Impaired working and short-term memory
• Slowed information processing
• Difficulty with planning, organization, and problem-solving
• Impaired language fluency

Personality changes may involve:

• Emotional instability
• Irritability
• Loss of social inhibition
• Apathy or lack of motivation
• Impulsivity
• Reduced empathy or insight

These effects are particularly associated with damage to the frontal lobes and often resemble frontal lobe syndromes seen in
degenerative diseases or tumors.

Patients may become unable to maintain employment, lose interpersonal relationships, and experience depression or anxiety
as they become aware of their limitations. Family and caregivers may report a sense that the person’s personality has changed
fundamentally.

A comprehensive neuropsychological assessment is crucial to identify specific impairments and to guide rehabilitation plans.
Rehabilitation After Head Injury

Rehabilitation is a vital component of recovery, beginning in the acute phase and continuing long into the chronic phase of
recovery. The goal is not only to maximize physical function but also to optimize cognitive, emotional, and social reintegration.

A coordinated multidisciplinary team is essential. This typically includes:

• Neurologists or rehabilitation physicians

• Neurosurgeons
• Neuropsychologists
• Physiotherapists
• Speech and language therapists
• Occupational therapists
• Psychiatrists or clinical psychologists
• Social workers and case managers

Key elements of rehabilitation involve:

• Motor training for weakness or coordination deficits

• Speech and communication therapy
• Memory retraining and attention exercises
• Behavioral therapy for aggression, impulsivity, or disinhibition
• Counseling and psychiatric support for mood disorders and adjustment issues
• Vocational rehabilitation and workplace reintroduction

Family involvement is crucial. Education and support must be provided to caregivers, who often face significant emotional and
practical challenges.

The duration and intensity of rehabilitation depend on:

• The severity of the initial injury

• The rate of spontaneous neurological recovery
• The presence of co-existing medical or psychiatric illness
• Patient motivation and family support

Although recovery plateaus after a certain point (often around 12–18 months), neuroplasticity allows for continued
improvements, especially with persistent therapeutic engagement.

Legal and Societal Considerations

Patients with persistent neurological deficits may require:

• Disability certification
• Legal guardianship
• Driving restrictions, particularly if seizures or cognitive deficits are present
• Supervised living arrangements

In many countries, patients with epilepsy or post-traumatic seizures must be seizure-free for a defined period (often 12 months)
before resuming driving.

Workplace reintegration may require:

• Modified duties
• Reduced hours
• Occupational health assessments

Long-term care needs and social security issues may need to be addressed through case management, benefits support, and
community services.
CRANIO-CEREBRAL INJURIES

(Head Injuries – Part 5: Long-Term Complications, Post-Traumatic Syndromes, and Rehabilitation)

Post-Traumatic Epilepsy

After a head injury, seizures may occur either in the immediate post-injury period or delayed, often weeks, months, or even
years later. The term post-traumatic epilepsy (PTE) refers specifically to recurrent, unprovoked seizures that occur after
traumatic brain injury.

Timing of Seizures:

• Immediate seizures occur within 24 hours of the injury and are usually a direct consequence of cortical irritation,
especially in open injuries, contusions, or penetrating trauma. These seizures do not necessarily predict later epilepsy.
• Early seizures occur within the first week and may reflect a greater degree of cortical damage. However, their presence
does not confirm that epilepsy will follow.
• Late post-traumatic seizures, occurring after more than 7 days, especially if repetitive or spontaneous, signify
epileptogenesis and typically meet the criteria for epilepsy.

Risk Factors for PTE:

• Penetrating head injuries

• Severe closed head injuries with depressed skull fractures
• Cortical contusions, especially multiple or hemorrhagic
• Intracerebral or subdural hematomas
• Prolonged loss of consciousness
• Early post-traumatic seizures
• Children and young adults are more susceptible to long-term epileptogenic changes than older adults.

Management:

• Prophylactic antiepileptic treatment, such as phenytoin or levetiracetam, may be given in the first 7 days to prevent
immediate or early seizures, especially in high-risk patients.
• There is no evidence that early prophylaxis prevents the development of long-term epilepsy.
• Once a patient develops late seizures, treatment follows the general principles of epilepsy management, with long-
term antiepileptic therapy tailored to seizure type and tolerability.

Post-Concussion Syndrome (PCS)

After a mild or moderate head injury, some patients experience a constellation of persistent symptoms not always accompanied
by visible structural brain damage. This group of symptoms is collectively referred to as post-concussion syndrome.

Clinical Features:

• Headache, often described as a dull ache or pressure

• Dizziness or imbalance
• Fatigue, frequently debilitating
• Irritability, emotional lability, anxiety, or low mood
• Concentration difficulties and impaired short-term memory
• Photophobia (light sensitivity) and phonophobia (sound sensitivity)
• Sleep disturbances, including insomnia or hypersomnia
Onset and Course:

Symptoms may begin immediately or within hours of the injury and typically resolve within weeks to months. However, in a
minority of patients, particularly those with underlying psychological vulnerability or compensation-related stress, symptoms
may persist much longer.

Pathophysiology:

The exact mechanism of PCS is not well understood. It is likely to be multifactorial, involving:

• Mild axonal disruption or metabolic dysfunction

• Psychological and emotional stress response
• Neurotransmitter imbalance

No single structural abnormality explains the syndrome, and imaging is often normal.

Management:

• Reassurance and education are the most important components.

• Patients should be informed that symptoms are real but usually self-limiting.
• Symptomatic treatment (e.g. for headaches or insomnia) may be needed.
• If symptoms persist beyond three months, neuropsychological support, physiotherapy, and occupational therapy may
be indicated.
• Antidepressants or anxiolytics may be used if mood symptoms dominate.

Cognitive and Neuropsychiatric Sequelae

Many patients recovering from traumatic brain injury—especially moderate to severe injuries—experience a variety of long-
term cognitive and behavioral disturbances. These sequelae can persist even when imaging appears normal, and may
profoundly affect quality of life and functional independence.

Cognitive Effects:

• Memory deficits, particularly for new learning

• Slowness of information processing
• Impaired attention and concentration
• Executive dysfunction, including planning, abstraction, and problem-solving
• Impaired language fluency in some cases

Behavioral and Psychiatric Changes:

• Emotional instability, including depression, irritability, and mood swings

• Apathy, or lack of motivation
• Social inappropriateness, impulsivity, or aggression
• Anxiety disorders, particularly generalized anxiety and PTSD
• Psychosis, though rare, may occur after severe injury or in vulnerable individuals

These changes are most pronounced when the frontal or temporal lobes are involved, and may arise even in the absence of
visible injury. Family members often recognize these changes before the patient does.

Assessment and Treatment:

• Comprehensive neuropsychological assessment is crucial for identifying specific deficits and planning intervention.
• Cognitive rehabilitation, speech therapy, and behavioral therapy can help regain function and develop coping
strategies.
• Psychiatric support with psychotherapy or pharmacological agents (e.g., SSRIs) may be necessary.
Rehabilitation and Recovery After Head Injury

Rehabilitation is a critical part of the long-term management of patients with traumatic brain injury. It must be multidisciplinary,
individualized, and initiated as early as the patient’s condition allows.

Core Goals:

• Maximize recovery of physical, cognitive, and psychological function

• Minimize disability and dependence
• Support return to work or education
• Educate family and caregivers
• Prevent secondary complications, such as pressure sores, contractures, or depression

Rehabilitation Team May Include:

• Physiatrist (rehabilitation specialist)

• Neurologist or neurosurgeon
• Neuropsychologist
• Physiotherapist
• Speech and language therapist
• Occupational therapist
• Social worker
• Psychiatrist or psychologist
• Nursing and support staff

Therapies must be tailored to:

• Severity of injury
• Age and pre-morbid function
• Specific deficits (e.g., motor, language, behavior)
• Personal and vocational goals

Rehabilitation is not linear and may require long periods of adjustment, especially in severe injury. Community-based programs,
day centers, and transitional facilities can help bridge the gap between hospital discharge and full reintegration into society.

Family Involvement:

Family members are crucial to both recovery and reintegration. They require:

• Clear communication
• Education about expectations and prognosis
• Emotional support

Conclusion of the Topic

Cranio-cerebral injuries are complex, with effects that range from full recovery to lifelong disability or death. Management must
be acute, proactive, and multidisciplinary, aiming not only to preserve life but to optimize long-term outcomes. Preventing
secondary injury, recognizing subtle signs, addressing psychological and social consequences, and guiding patients through
rehabilitation are all essential for comprehensive care.
VASCULAR DISEASES OF THE SPINAL CORD

(Part 1: Vascular Anatomy and Infarction Syndromes)

Blood Supply of the Spinal Cord: Anatomical Overview

The vascular supply of the spinal cord is anatomically complex and relies on both longitudinal arteries and segmental
anastomotic feeders to maintain adequate perfusion.

Main Arteries:

• The anterior spinal artery is formed from branches of the vertebral arteries, which unite to form a single longitudinal
vessel running within the anterior median fissure of the spinal cord.
• The posterior spinal arteries usually arise from the posterior inferior cerebellar arteries and form a plexiform network
over the posterior surface of the cord.

Both systems run the entire length of the spinal cord and are supplemented by radicular arteries from segmental levels.

Radicular Arteries:

• The posterior spinal artery plexus is reinforced by approximately 12 unpaired posterior radicular arteries, which
provide a rich collateral network. This explains why the posterior one-third of the spinal cord, including the dorsal
columns, is relatively protected from ischemia.
• The anterior spinal artery is more vulnerable, with only 7–10 anterior radicular arteries, mostly entering from the left
side, and with poorer collateral circulation.

Segmental Contributions:

• Cervical radicular arteries arise from the vertebral and subclavian arteries.
• Intercostal arteries supply the thoracic segments.
• The artery of Adamkiewicz, the largest radicular artery, usually arises between T9 and L2, and is found on the left side
in 70% of individuals. It plays a key role in perfusing the lower thoracic and lumbar spinal cord.
• Sacral levels are supplied by arteries branching from the hypogastric system.

Watershed Vulnerability:

The narrowest point of the anterior spinal artery lies at T8, making this region a watershed zone especially susceptible to
ischemia, particularly in settings of hypotension or systemic vascular compromise.

Territories Supplied by the Spinal Arteries

• Posterior Spinal Artery Territory:

o Supplies the posterior one-third of the spinal cord, including:
§ Dorsal columns (fasciculus gracilis and cuneatus)
§ Some parts of the posterior horn
• Anterior Spinal Artery Territory:
o Supplies the anterior two-thirds of the spinal cord through:
§ Penetrating branches to the anterior and part of posterior grey matter
§ Circumferential branches to the anterior and lateral white matter, including:
§ Corticospinal tracts
§ Spinothalamic tracts
There is virtually no anastomotic communication between the anterior and posterior systems. Hence, infarction in the territory
of the anterior spinal artery tends to produce more severe clinical consequences than posterior infarction.

Vascular Syndromes of the Spinal Cord

Anterior Spinal Artery Syndrome

This is the most common ischemic syndrome of the spinal cord and results from infarction within the anterior spinal artery
territory.

Clinical Features:

• Radicular pain at onset

• Sudden onset paraparesis or quadriparesis
• Initial flaccid paralysis due to spinal shock, evolving into spasticity
• Areflexia, which transitions over days to hyperreflexia and Babinski signs
• Dissociated sensory loss:
o Loss of pain and temperature sensation below the lesion (spinothalamic tract involvement)
o Preservation of vibration and joint position sense (dorsal columns spared)
• Bladder dysfunction, commonly urinary retention

When only the penetrating branches of the anterior spinal artery are affected, the damage may selectively involve the anterior
horn cells or long tracts, with minimal sensory symptoms.

Infarction in the anterior spinal artery territory may occur slowly in the context of aortic atheroma, often producing selective
anterior horn cell damage. In rare cases, a pure conus medullaris syndrome may be the result.

Posterior Spinal Artery Syndrome

This is a much rarer condition, owing to the robust collateral circulation of the posterior spinal arterial system.

Clinical Features:

• Loss of joint position sense (proprioception)

• Sensory ataxia
• Weakness or loss of tendon reflexes
• In advanced cases, ischemia may extend into the posterior grey horns

Venous Infarction

Venous infarction of the spinal cord is an uncommon but catastrophic event, typically occurring in the context of pelvic sepsis,
or venous outflow obstruction. It may present as a complete cord syndrome with:

• Sudden paraplegia
• Rapid progression
• Poor neurological recovery

This condition is often fatal or results in severe permanent disability.

VASCULAR DISEASES OF THE SPINAL CORD

(Part 2: Arteriovenous Malformations, Spinal Hemorrhage, and Investigation)

Spinal Arteriovenous Malformations (AVMs)

Spinal arteriovenous malformations represent a congenital or acquired vascular anomaly, characterized by direct
communication between arterial and venous channels without an intervening capillary bed. These abnormal vascular
connections can lead to spinal cord dysfunction through several mechanisms:

• Venous hypertension, leading to chronic cord congestion

• Ischemia due to shunting of blood away from normal capillaries
• Bleeding into the spinal cord or subarachnoid space

Spinal AVMs are relatively rare and may not present until adulthood, although they are congenital in origin.

Types of Spinal AVMs

Spinal arteriovenous malformations are broadly classified into:

1. Dural AV Fistulas (Type I):

o These are the most common type, usually acquired in adulthood.
o The abnormal communication is between a radicular artery and a radicular vein within the dural sleeve.
o These fistulas create arterialization of the venous system, leading to venous hypertension and subsequent
spinal cord congestion and ischemia.
o Symptoms develop insidiously and progressively, without acute hemorrhage.
2. Intradural AVMs (Types II–IV):
o These occur within the spinal cord parenchyma or pial surface.
o They often affect young adults or children.
o Present with either:
§ Subacute myelopathy due to chronic ischemia, or
§ Sudden neurologic deterioration due to intramedullary or subarachnoid hemorrhage

Clinical Presentation of Spinal AVMs

The symptoms vary depending on the type, location, and hemodynamic behavior of the malformation.

Patients may present with:

• Progressive weakness, especially in the legs

• Gait unsteadiness
• Sensory deficits, often involving pain and temperature modalities
• Sphincter disturbance, including urinary incontinence or retention
• Back or radicular pain
• Sudden deterioration with pain and neurological deficit if hemorrhage occurs

In dural AV fistulas, symptoms evolve slowly, often misdiagnosed as demyelination or spinal stenosis.
Spinal Hemorrhages

Spinal hemorrhages are less common than cerebral bleeds but are equally serious. They may occur in various spaces, each with
its own implications:

Spinal Subarachnoid Hemorrhage

• Usually results from rupture of an AVM, less commonly from trauma or coagulopathy
• Presents with:
o Sudden back pain
o Radicular pain
o Rapid onset of neurological signs such as paraplegia or sensory level
• May be associated with meningeal signs if blood extends cranially
• CSF analysis shows:
o Blood in the CSF
o Xanthochromia
o Elevated opening pressure

Spinal Subdural Hematoma

• Rare condition
• Most commonly related to:
o Trauma
o Anticoagulation therapy
o Spinal anesthesia
• Presents acutely with:
o Severe back pain
o Rapid neurological deterioration

Diagnosis is made via MRI, and treatment often involves surgical decompression.

Spinal Epidural Hematoma

• May arise spontaneously in patients on anticoagulants or with bleeding disorders

• Can also follow trauma or epidural injections
• Presents with:
o Acute onset back pain
o Radicular symptoms
o Spinal cord or cauda equina compression
• MRI shows a space-occupying lesion compressing the thecal sac
• Urgent surgical decompression is often required to preserve function

Investigation of Spinal Cord Vascular Lesions

A thorough clinical evaluation must be followed by targeted imaging and diagnostic studies, tailored to the suspected vascular
lesion.
MRI

• The investigation of choice for suspected spinal cord infarction, AVMs, and hemorrhage
• Demonstrates:
o Signal changes in the cord
o Flow voids suggesting vascular malformation
o Hematomas and their anatomical relationships
• Contrast-enhanced MRI may help to delineate abnormal vascular networks

Spinal Angiography

• Digital subtraction angiography (DSA) remains the gold standard for detailed vascular imaging
• Required to:
o Precisely define the arterial supply and venous drainage of AVMs
o Locate feeding vessels and nidus in AVMs
o Plan surgical or endovascular intervention
• May involve selective catheterization of vertebral, intercostal, and lumbar arteries

CSF Examination

• Performed in cases of suspected subarachnoid hemorrhage

• Will reveal:
o Xanthochromia (if blood has been present for several hours)
o Elevated protein content in venous congestion syndromes
o May exclude inflammatory or demyelinating disorders

Evoked Potentials and Electrophysiology

• May support diagnosis when imaging is equivocal

• Somatosensory evoked potentials (SSEPs) may show impaired conduction in infarction or compression

Management Principles

Management strategies depend on the nature and urgency of the vascular lesion.

• Anterior spinal artery infarction: supportive care, prevent complications, manage bladder and rehabilitation
• AVMs:
o Endovascular embolization: especially for dural fistulas or small AVMs
o Microsurgical resection: for accessible lesions
o Stereotactic radiosurgery: for small, deep malformations
• Hemorrhages:
o Immediate surgical evacuation for epidural or subdural hematomas
o Correction of coagulopathy
o Blood pressure management and supportive care in subarachnoid bleeds
VASCULAR DISEASES OF THE BRAIN

(Part 1: Introduction, Risk Factors, and Mechanisms of Cerebrovascular Disease)

General Overview

Vascular diseases of the brain, collectively termed cerebrovascular diseases, are among the most frequent causes of hospital
admission in neurological practice. They are a leading cause of disability and death worldwide. In the United Kingdom, for
instance, the annual incidence varies by region between 150 and 200 cases per 100,000 population, while the prevalence is
approximately 600 per 100,000. Notably, about one-third of these individuals are severely disabled as a result of the vascular
event.

Despite improvements in medical therapy, cerebrovascular disease remains the third leading cause of death in developed
countries, following heart disease and cancer.

Preventive Strategies and Risk Factors

Preventing cerebrovascular disease is far more effective in reducing mortality and disability than treating it after it occurs.
Therefore, identifying and managing modifiable risk factors is of critical importance.

Age

• Increasing age is the most significant non-modifiable risk factor.

• The risk of vascular events increases progressively with age and cannot be corrected, but it does emphasize the
importance of prevention in older populations.

Hypertension

• Hypertension is the most important modifiable factor and is implicated in both thrombotic infarctions and intracranial
hemorrhages.
• Risk correlates directly with the level of blood pressure, and there is no clear-cut threshold below which the risk
disappears.
• A reduction of 6 mmHg in diastolic blood pressure is associated with a 40% reduction in fatal and non-fatal strokes.
• Even systolic hypertension, especially in the elderly, is now recognized as clinically significant and no longer considered
benign.

Cardiac Disease

Several cardiac abnormalities predispose to stroke, particularly through embolic events:

• Cardiac enlargement
• Heart failure
• Cardiac arrhythmias, particularly atrial fibrillation
• Rheumatic heart disease
• Patent foramen ovale
• Rare conditions such as atrial myxoma

Diabetes Mellitus

• Doubles the risk of cerebral infarction.

• Improved glycemic control has not yet demonstrated a significant reduction in the incidence of atherosclerotic
complications.
Hereditary Factors

• First-degree relatives of patients with stroke are at only a slightly increased risk compared to the general population.
• Familial trends for diabetes and hypertension can complicate interpretation of pure genetic risk.

Blood Lipids, Cholesterol, Smoking, and Obesity

• These are less strongly associated with cerebrovascular disease than with coronary artery disease.
• Nonetheless, they still contribute to the overall vascular burden, especially in combination.

Ethnicity and Geography

• Apparent racial differences are believed to reflect lifestyle, diet, and environmental exposures, more than true genetic
susceptibility.

Haematological Factors

• High hematocrit or elevated hemoglobin concentration is associated with increased stroke risk.
• Other contributing haematologic abnormalities include reduced fibrinolysis and coagulopathies.

Oral Contraceptives

• High-dose combined oral contraceptives (COCs) containing oestrogen significantly increase thrombotic risk.
• The effects of modern low-dose formulations remain less clear but are considered safer, particularly in non-smokers.

Mechanisms of Cerebrovascular Disease

While "stroke" is a broad clinical term that lacks pathological precision, cerebrovascular disease is defined as any brain
dysfunction resulting from abnormalities of the cerebral blood vessels or blood flow. The major pathophysiological
mechanisms include:

1. Vascular Occlusion
o Caused by thrombosis (clot formation at the site) or embolism (clot or debris traveling from another site).
o Leads to cerebral ischemia and infarction.
2. Vessel Wall Rupture
o Results in haemorrhagic stroke, either into brain parenchyma (intracerebral haemorrhage) or into the
subarachnoid space.
3. Primary Disease of the Vessel Wall
o Includes atherosclerosis, vasculitis, fibromuscular dysplasia, and collagen vascular disorders.
o May cause stenosis, occlusion, or aneurysm formation.
4. Abnormalities in Blood Constituents
o Disorders of coagulation, blood viscosity, or cellular elements may promote thrombosis or hemorrhage.
o Examples include polycythemia, thrombophilia, antiphospholipid syndrome, and sickle cell disease.

Resulting Pathologies

All of the above mechanisms ultimately result in:

• Cerebral infarction due to ischemia (∼85% of all strokes)

• Cerebral haemorrhage, either parenchymal or subarachnoid (∼15% of all strokes)

The impact of these vascular events depends on:

• The location and size of the lesion

• The age and health of the patient
 • The underlying cause
• The level of consciousness at admission, which serves as a prognostic indicator

VASCULAR DISEASES OF THE BRAIN

(Part 2: Natural History, Types of Stroke, and Vascular Occlusion Mechanisms)

Natural History of Cerebral Infarction

Cerebral infarction, caused by interruption of arterial blood flow to part of the brain, may evolve in several patterns depending
on multiple factors such as:

• The size and location of the affected vessel

• The availability of collateral circulation
• The duration of ischemia
• The timeliness of reperfusion

Types of Evolution:

1. Sudden onset with no progression

o Common in embolism, where a clot abruptly occludes a cerebral artery.
o The neurological deficit appears instantaneously and remains unchanged thereafter.
2. Stuttering progression over hours to days
o More typical of in-situ thrombosis, particularly over a background of atherosclerosis.
o The patient may experience stepwise worsening or fluctuating symptoms.
3. Transient ischemic attacks (TIAs)
o Defined as neurological deficits resolving completely within 24 hours.
o TIAs are an important warning sign, especially when they are recurrent or follow a stereotyped pattern.
o They often precede a full stroke and require urgent intervention to prevent permanent damage.

Aetiology of Cerebral Infarction

The mechanisms by which cerebral infarction occurs include:

1. Thrombosis

Thrombosis refers to the local formation of a clot within a cerebral artery, typically occurring in arteries already narrowed by
atherosclerosis.

Sites and Characteristics:

• Most common in the internal carotid artery bifurcation, the origin of the middle cerebral artery (MCA), or
vertebrobasilar system.
• The clot often develops gradually, over minutes to hours.
• The clinical picture often reflects lacunar infarcts, watershed infarcts, or territorial infarcts.
Predisposing Factors:

• Atherosclerosis, especially with plaque ulceration

• Hypercoagulable states
• Inflammatory vasculopathies
• Hypoperfusion, especially in regions with poor collateral supply

2. Embolism

Embolic strokes are caused by particles or debris that originate from a distant source and travel through the bloodstream,
eventually occluding a cerebral artery.

Common Sources:

• Cardiac emboli (the most common cause):

o Atrial fibrillation (especially non-valvular)
o Myocardial infarction with mural thrombus
o Prosthetic heart valves
o Rheumatic mitral valve disease
o Patent foramen ovale
o Atrial myxoma
• Artery-to-artery embolism:
o Atherosclerotic plaque fragments may dislodge from the carotid arteries, aortic arch, or vertebral arteries.
• Paradoxical embolism:
o Venous thromboemboli pass through a right-to-left cardiac shunt (e.g., patent foramen ovale), bypassing the
lungs.

Clinical Features:

• Abrupt onset of focal deficits.

• Deficits may vary depending on the embolus location:
o Middle cerebral artery (MCA) embolism: contralateral hemiplegia, hemisensory loss, gaze preference, aphasia
(if dominant hemisphere).
o Posterior cerebral artery (PCA) embolism: visual field loss.
• Multiple emboli may cause multifocal infarcts in different vascular territories.

3. Haemodynamic Hypoperfusion

Infarction may occur not from occlusion but from critically reduced cerebral perfusion, especially in the presence of systemic
hypotension or carotid occlusion.

This type of ischemia most commonly affects watershed zones, also known as border zones, which lie between the territories of
major cerebral arteries (e.g., ACA-MCA or MCA-PCA junctions).

Typical Causes:

• Cardiac arrest
• Severe hypotension
• Carotid stenosis with inadequate collateral flow

Symptoms:

• Bilateral symptoms may occur in severe hypoperfusion (e.g., cortical blindness).

• Often produces diffuse or symmetrical infarcts, unlike focal strokes from thrombosis or embolism.
4. Lacunar Infarction

Lacunar infarcts are small (<15 mm) infarcts occurring in the deep structures of the brain, such as the:

• Basal ganglia
• Internal capsule
• Thalamus
• Pons
• Deep white matter

They result from occlusion of small penetrating arteries, often due to lipohyalinosis or microatheroma, typically in the setting
of chronic hypertension or diabetes mellitus.

Typical Clinical Syndromes:

• Pure motor hemiparesis

• Pure sensory stroke
• Sensorimotor stroke
• Ataxic hemiparesis
• Dysarthria–clumsy hand syndrome

Lacunar infarcts often do not produce cortical signs such as aphasia or visual field deficits. Despite their small size, multiple
lacunes may accumulate and contribute to vascular dementia.

5. Arterial Dissection

Arterial dissection involves a tear in the vessel wall, leading to intramural hematoma and luminal narrowing or occlusion. It
often affects:

• The extracranial internal carotid artery

• The vertebral artery

Etiology:

• May be spontaneous, traumatic, or related to connective tissue disorders such as Ehlers-Danlos syndrome or
fibromuscular dysplasia.

Clinical Features:

• Neck pain or headache, often unilateral

• Partial Horner’s syndrome
• Cranial nerve palsies (e.g., hypoglossal nerve)
• Subsequent ischemic stroke in the affected vascular territory

Diagnosis is made via MRI with fat suppression, MRA, or CT angiography.

VASCULAR DISEASES OF THE BRAIN

(Part 2 – Continued: Natural History of Infarction, Classification by Cause)

Natural History of Infarction (continued)

2. Sudden onset with progression over minutes or hours

This pattern is frequently seen in patients with thrombotic infarction, especially when arising from large vessel
occlusion in the context of atheromatous disease.
The symptoms typically begin abruptly but worsen gradually as the thrombus propagates or as perfusion diminishes
further due to falling systemic pressure or growing infarct volume.
3. Stepwise progression over hours or days
This is usually due to small vessel disease, involving the deep penetrating arteries, as in lacunar infarctions.
The evolving picture may mimic a series of transient ischemic attacks that become progressively incomplete, until a
more permanent neurological deficit is established.
4. Fluctuating course
Fluctuating deficits may occur when there is incomplete occlusion, collateral circulation, or systemic factors such as
hypotension or hypoxia influencing perfusion.
This course may be seen in patients with carotid stenosis or border-zone infarcts.
The deficits worsen and improve, often correlating with posture or blood pressure, and sometimes with therapeutic
intervention.
5. Stuttering deterioration followed by improvement
In some cases, a reperfusion event may restore flow before infarction becomes complete.
In others, cytotoxic edema may resolve spontaneously, or collateral flow may compensate, leading to partial recovery.
Rarely, patients may develop secondary hemorrhagic transformation of the infarcted area during this stage of
spontaneous or therapeutic reperfusion.

Pathological Types of Infarction

Cerebral infarcts can be classified histologically and grossly into:

• Pale (anemic) infarcts

These are associated with thrombotic occlusion, usually of large arteries like the middle cerebral artery.
The occlusion leads to cessation of blood flow with no reperfusion.
The tissue undergoes coagulative necrosis, evolving into a cystic cavity over several weeks.
• Red (hemorrhagic) infarcts
These typically result from embolism, especially when reperfusion occurs into infarcted tissue.
The infarcted area becomes soft, swollen, and stained with blood.
This type of infarct is more prone to causing secondary bleeding, particularly if the patient is anticoagulated.

In both types, the infarcted tissue evokes an inflammatory response, followed by liquefactive necrosis, and eventually gliosis or
encephalomalacia (softening of the brain).

Thrombosis, Embolism, and Hemorrhage: Classification by Cause

Cerebrovascular disease can be further classified by the underlying vascular mechanism:

Thrombosis

Thrombosis refers to the formation of a blood clot at the site of an atherosclerotic plaque, which partially or completely
occludes the lumen of a cerebral artery.

Typical Features:

• More common in older patients

• Often associated with hypertension, diabetes, and hyperlipidemia
• Often preceded by transient ischemic attacks (TIAs)

Sites Most Frequently Affected:

• Carotid bifurcation
• Origin of the middle cerebral artery
• Vertebral artery origins
• Basilar artery

Clinical Features:

• Stroke develops gradually, often at night or in the early morning

• Fluctuating symptoms or stepwise deterioration are characteristic
• Symptoms correlate with the territory supplied by the affected artery

Pathological Findings:

• The lumen of the artery is narrowed by atherosclerotic plaque

• Platelet-fibrin thrombus overlies the plaque
• Distal infarction is typically pale, with variable edema and swelling

Embolism

An embolism refers to the sudden occlusion of a cerebral artery by material that has travelled from a distant site, most often
the heart or large extracranial arteries.

Common Sources of Emboli:

• Cardiac thrombi, especially in atrial fibrillation, valvular disease, or recent myocardial infarction
• Vegetations in infective endocarditis
• Fat, air, or tumor emboli (rare)
• Atheromatous debris from the aortic arch or carotid arteries

Typical Features:

• Onset is sudden, often during activity or stress

• Deficit appears maximally at onset
• Seizures may occur, especially if cortical tissue is involved
• Emboli often lodge at arterial bifurcations, especially in the middle cerebral artery

Pathological Findings:

• The infarct is often hemorrhagic, particularly if spontaneous or therapeutic reperfusion occurs

• Emboli may fragment, causing multiple small infarcts in the same or different vascular territories
Hemorrhage

Cerebral hemorrhage occurs when a blood vessel ruptures, spilling blood into the brain parenchyma or subarachnoid space.

Types of Hemorrhage:

• Intracerebral hemorrhage: bleeding into brain tissue

• Subarachnoid hemorrhage: bleeding into the subarachnoid space, often from a ruptured aneurysm
• Intraventricular hemorrhage: bleeding into the ventricular system
• Subdural/epidural hemorrhage: associated more with trauma than vascular disease

Causes of Intracerebral Hemorrhage:

• Chronic hypertension causing rupture of small penetrating arteries

• Cerebral amyloid angiopathy in the elderly
• Arteriovenous malformations
• Coagulopathy or anticoagulant therapy
• Vasculitis or aneurysmal rupture (rare for intraparenchymal bleeds)

Clinical Features:

• Often occurs during exertion or emotional stress

• Sudden onset of headache, vomiting, and rapid neurological deterioration
• Common sites:
o Basal ganglia
o Thalamus
o Pons
o Cerebellum

Imaging and Pathology:

• CT scan shows hyperdense (bright) area corresponding to blood

• Hemorrhage may extend into the ventricles
• Mass effect and midline shift may cause rapid herniation and death
VASCULAR DISEASES OF THE BRAIN

(Part 3: Transient Ischemic Attacks and Clinical Stroke Syndromes by Vascular Territory)

Transient Ischemic Attacks (TIAs)

Transient Ischemic Attacks (TIAs) are characterized by sudden neurological deficits that resolve completely within 24 hours and
are presumed to be due to temporary cerebral ischemia. Although the formal time threshold remains at 24 hours, in modern
clinical usage the term often refers to deficits that last only a few minutes to a few hours, without radiologic evidence of
infarction.

TIAs are an important clinical entity because they serve as warning signs of impending infarction. A significant proportion of
strokes—especially thrombotic strokes—are preceded by TIAs, sometimes with recurrent stereotyped episodes.

Mechanisms of TIAs:

• Platelet emboli originating from an ulcerated atheromatous plaque

• Microthrombi in narrowed arteries
• Haemodynamic insufficiency, especially in the presence of carotid stenosis
• Artery-to-artery embolism
• In rare cases, cardiogenic emboli that lyse spontaneously or fail to completely occlude a distal vessel

Clinical Patterns of TIAs:

TIAs may be classified according to the vascular territory affected. Common presentations include:

1. Carotid Territory TIAs:

o Unilateral weakness or numbness, usually affecting the face, arm, or leg
o Dysphasia, if the dominant hemisphere is involved
o Transient monocular blindness (amaurosis fugax), due to retinal ischemia
2. Vertebrobasilar Territory TIAs:
o Bilateral weakness or numbness
o Vertigo, diplopia, dysarthria, or dysphagia
o Drop attacks, especially with cerebellar or brainstem ischemia

These episodes are usually brief (lasting less than 1 hour) and leave no residual signs. However, recurrence—especially with
increasing frequency—requires urgent investigation and intervention to prevent full infarction.

Clinical Stroke Syndromes by Vascular Territory

Understanding the specific cerebral vascular territories is critical for localizing stroke lesions and identifying the underlying
vascular pathology. The clinical features of a stroke depend on which artery is occluded and which part of the brain is affected.

Middle Cerebral Artery (MCA) Territory

The middle cerebral artery is the most frequently involved vessel in cerebral infarction, largely due to its direct continuation
from the internal carotid artery.
Structures Supplied:

• Most of the lateral convexity of the cerebral hemisphere

• Motor and sensory cortex for face and arm
• Broca’s and Wernicke’s areas in the dominant hemisphere
• Optic radiations (temporal and parietal lobes)
• Basal ganglia via lenticulostriate branches

Clinical Features of MCA Infarction:

• Contralateral hemiplegia and hemisensory loss, face and arm more affected than leg
• Aphasia:
o Broca’s aphasia (non-fluent, expressive) if anterior MCA branch is involved
o Wernicke’s aphasia (fluent, receptive) if posterior branch is involved
o Global aphasia in large MCA strokes
• Homonymous hemianopia or quadrantanopia
• Gaze deviation towards the side of the lesion (due to frontal eye field involvement)
• Hemineglect or anosognosia in non-dominant hemisphere lesions

MCA infarcts often result in extensive disability, especially in the dominant hemisphere.

Anterior Cerebral Artery (ACA) Territory

The anterior cerebral artery arises from the internal carotid and courses medially to supply the medial aspects of the frontal
and parietal lobes, particularly the superior parts of the sensorimotor cortex.

Structures Supplied:

• Medial frontal lobe

• Paracentral lobule (motor and sensory cortex for leg)
• Corpus callosum
• Part of the cingulate gyrus

Clinical Features of ACA Infarction:

• Contralateral weakness and sensory loss predominantly affecting the lower limb
• Urinary incontinence due to medial frontal lobe involvement
• Abulia (lack of initiative), apathy, or mutism
• Grasp reflex and other frontal release signs
• Rarely, paraplegia if both ACAs are involved (e.g. in an unpaired ACA trunk)

ACA strokes are less common than MCA strokes but may cause significant disability, especially in bilateral involvement.

Posterior Cerebral Artery (PCA) Territory

The posterior cerebral artery arises from the basilar artery and supplies the occipital lobe, inferior temporal lobe, and
posterior corpus callosum.

Structures Supplied:

• Primary visual cortex in the occipital lobe

• Medial temporal lobe structures (including hippocampus)
• Thalamus via perforating branches
Clinical Features of PCA Infarction:

• Contralateral homonymous hemianopia, often macula-sparing

• If dominant hemisphere is involved:
o Alexia without agraphia (inability to read with preserved writing), from damage to the left visual cortex and
splenium of the corpus callosum
• Visual agnosias or prosopagnosia (inability to recognize faces)
• Memory impairment from hippocampal involvement
• Sensory loss or thalamic pain syndrome if thalamic branches are involved

Lacunar Syndromes (Small Vessel Disease)

Lacunar infarctions are small (<15 mm) infarcts resulting from occlusion of deep penetrating arteries, most often due to
hypertensive small vessel disease or lipohyalinosis.

Common Sites:

• Internal capsule
• Thalamus
• Basal ganglia
• Pons

Typical Lacunar Syndromes:

• Pure motor hemiparesis (internal capsule or basis pontis)

• Pure sensory stroke (thalamus)
• Ataxic hemiparesis
• Clumsy hand–dysarthria syndrome

These syndromes are not accompanied by cortical signs such as aphasia, neglect, or visual field deficits, distinguishing them
from cortical infarcts.
VASCULAR DISEASES OF THE BRAIN

(Part 4: Brainstem and Cerebellar Syndromes, Vertebrobasilar Occlusion, and Subarachnoid Hemorrhage)

Brainstem Syndromes

The brainstem contains densely packed ascending and descending tracts, along with the cranial nerve nuclei, and is supplied by
branches of the vertebrobasilar system. Infarctions in this area cause complex clinical syndromes involving crossed findings
(cranial nerve deficits on one side, motor or sensory deficits on the other).

General Characteristics:

• Cranial nerve palsies (e.g., III–XII) are common

• Contralateral hemiparesis or hemisensory loss
• Vertigo, diplopia, nystagmus, and ataxia are common signs of posterior circulation involvement
• Syndromes are often named eponymously based on anatomical localization

Lateral Medullary Syndrome (Wallenberg’s Syndrome)

Caused by occlusion of the posterior inferior cerebellar artery (PICA) or vertebral artery, affecting the lateral medulla.

Clinical Features:

• Ipsilateral loss of pain and temperature on the face (spinal trigeminal nucleus)
• Contralateral loss of pain and temperature on the body (spinothalamic tract)
• Ipsilateral Horner's syndrome (ptosis, miosis, anhidrosis)
• Ataxia (inferior cerebellar peduncle)
• Nystagmus, vertigo, and vomiting
• Dysphagia, dysarthria, and hoarseness (nucleus ambiguus involvement)
• Ipsilateral palatal and vocal cord paralysis

This syndrome is distinctive in its crossed sensory findings and involvement of bulbar functions.

Medial Medullary Syndrome (Dejerine Syndrome)

Due to infarction in the anterior spinal artery affecting the medial medulla.

Clinical Features:

• Contralateral hemiparesis (corticospinal tract)

• Contralateral loss of proprioception and fine touch (medial lemniscus)
• Ipsilateral tongue weakness (hypoglossal nerve palsy)
Pontine Syndromes

The pons is supplied by branches of the basilar artery.

• Medial pontine infarction affects the corticospinal tract, medial lemniscus, and abducens nucleus
o Leads to contralateral hemiparesis, loss of proprioception, and ipsilateral lateral rectus palsy
• Lateral pontine infarction may involve:
o Facial nerve nucleus (facial palsy)
o Vestibular nuclei (vertigo, nystagmus)
o Spinal trigeminal nucleus and spinothalamic tract (crossed pain and temperature loss)

These syndromes often manifest with gaze palsies, facial weakness, and ataxia, depending on the precise arterial territory
affected.

Cerebellar Syndromes

The cerebellum receives blood from three main arteries:

• Superior cerebellar artery (SCA)

• Anterior inferior cerebellar artery (AICA)
• Posterior inferior cerebellar artery (PICA)

Infarction in the cerebellum produces:

• Ipsilateral limb ataxia

• Dysmetria
• Gait unsteadiness
• Dysarthria
• Vertigo and vomiting
• Nystagmus

Massive cerebellar infarctions may lead to compression of the brainstem, hydrocephalus, or tonsillar herniation, requiring
surgical decompression.

Vertebrobasilar Artery Occlusion

Occlusion of the vertebral arteries, basilar artery, or their branches can lead to widespread brainstem and cerebellar
dysfunction.

Vertebral Artery Occlusion:

• May cause Wallenberg syndrome

• Can also lead to bilateral cerebellar signs, vertigo, and neck pain

Basilar Artery Occlusion:

This is one of the most catastrophic vascular events, with very high morbidity and mortality.

Clinical Presentation:

• Vertigo, dizziness, nausea, and vomiting

• Bilateral motor signs: quadriplegia or hemiplegia
• Facial diplegia, dysarthria, and dysphagia
• Oculomotor disturbances: horizontal gaze palsy, internuclear ophthalmoplegia
• Consciousness disturbance: from drowsiness to coma
• Progression may lead to the locked-in syndrome
Locked-In Syndrome

This syndrome results from a bilateral infarction of the ventral pons, often due to basilar artery thrombosis.

Clinical Characteristics:

• Quadriplegia and anarthria (inability to speak)

• Preserved consciousness
• Preserved vertical eye movements and blinking, allowing yes/no communication
• Patients are aware and cognitively intact but are unable to move or speak

Diagnosis is often delayed because the patient cannot express themselves, and the preserved vertical eye movement may be
the only clue to intact awareness.

Prognosis is generally poor, though some patients survive with varying degrees of residual disability.

Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage refers to bleeding into the subarachnoid space, most often due to rupture of a cerebral aneurysm. It
constitutes a medical emergency with a high early mortality and risk of rebleeding, vasospasm, and hydrocephalus.

Causes of SAH:

• Ruptured saccular (berry) aneurysm: accounts for the majority of non-traumatic SAH
• Arteriovenous malformations (AVMs)
• Extension of intracerebral hemorrhage
• Bleeding diathesis or anticoagulation
• Trauma (the most common overall cause of SAH)
VASCULAR DISEASES OF THE BRAIN

(Part 5: Subarachnoid Hemorrhage, Berry Aneurysms, Arteriovenous Malformations)

Subarachnoid Hemorrhage (SAH)

Subarachnoid hemorrhage refers to the extravasation of blood into the subarachnoid space, which lies between the arachnoid
and pia mater, surrounding the brain and spinal cord. This condition presents as a medical emergency and requires rapid
recognition and intervention.

Causes of Spontaneous Subarachnoid Hemorrhage

The primary cause of non-traumatic SAH is the rupture of a cerebral (berry) aneurysm. Other causes include:

• Arteriovenous malformations (AVMs)

• Extension of intracerebral hemorrhage into the subarachnoid space
• Coagulopathies or anticoagulant use
• Cerebral vasculitis
• Cavernous angiomas
• Rarely, mycotic aneurysms or neoplastic bleeding

Trauma is the most frequent overall cause of SAH but is not classified with the spontaneous vascular forms.

Clinical Features of SAH

The classic presentation of SAH is with sudden, severe headache, often described as “the worst headache of my life.” The
headache reaches peak intensity within seconds to minutes, and is usually occipital or diffuse.

Associated features may include:

• Vomiting
• Photophobia
• Neck stiffness due to meningeal irritation
• Loss of consciousness, either transient or prolonged
• Seizures
• Focal neurological signs if the hemorrhage is asymmetric or involves adjacent brain tissue

In some cases, a sentinel headache or warning bleed occurs days or weeks before the major hemorrhage. This may be
overlooked unless specifically elicited in history.

Complications of Subarachnoid Hemorrhage

Subarachnoid hemorrhage is associated with several early and late complications, each contributing to morbidity and mortality.

1. Rebleeding

• The greatest risk occurs within the first 24 hours following the initial rupture.
• Rebleeding leads to higher mortality, especially before aneurysm clipping or coiling.
• Prevention includes early surgical intervention.
2. Cerebral Vasospasm

• Occurs in approximately 30–70% of patients after SAH, typically 4 to 10 days post-hemorrhage.

• Caused by irritation from subarachnoid blood, leading to arterial narrowing, reduced cerebral perfusion, and delayed
ischemic deficits.
• Clinical signs may include:
o Focal deficits
o Confusion
o Reduced level of consciousness
• Treatment includes:
o Nimodipine (a calcium channel blocker) to reduce risk
o Blood pressure elevation, volume expansion, and hemodynamic therapy

3. Hydrocephalus

• Blood in the subarachnoid space can block arachnoid granulations or obstruct CSF pathways, resulting in acute or
chronic hydrocephalus.
• Presents with:
o Headache
o Vomiting
o Drowsiness
o Papilledema
• Treated with:
o External ventricular drainage
o Long-term ventriculoperitoneal shunting if persistent

4. Hyponatremia

• Often occurs from cerebral salt wasting or, less commonly, SIADH
• Can lead to confusion and exacerbate cerebral edema
• Requires careful management of fluid balance and sodium replacement

5. Cardiac Complications

• SAH can cause ECG changes, arrhythmias, and myocardial stunning

• Attributed to catecholamine surge from hypothalamic stimulation

Berry Aneurysms

Berry aneurysms are saccular outpouchings that develop at arterial bifurcations within the circle of Willis. They are present in
1–2% of the population and may be asymptomatic until rupture.

Common Locations:

• Anterior communicating artery

• Posterior communicating artery
• Middle cerebral artery bifurcation

Predisposing Factors:

• Hypertension
• Smoking
• Polycystic kidney disease
• Connective tissue disorders (e.g., Ehlers-Danlos syndrome)
• Family history of aneurysms or SAH
Clinical Course:

• May remain silent for life

• Risk of rupture increases with size, location, and symptomatic presentation

Investigation of SAH and Aneurysms

When SAH is suspected, immediate and systematic investigation is essential.

1. CT Scan (Non-contrast)

• First-line investigation
• Highly sensitive for acute blood within the first 24 hours
• Identifies blood in basal cisterns, sulci, ventricles

2. Lumbar Puncture

• Performed if CT is negative but suspicion remains high

• Must wait at least 6–12 hours to allow development of xanthochromia
• CSF may show:
o Elevated opening pressure
o Blood-stained CSF (uniform in all tubes)
o Xanthochromia indicating bilirubin breakdown products

3. Cerebral Angiography

• Gold standard for identifying the source of bleeding

• Digital Subtraction Angiography (DSA) visualizes:
o Aneurysms
o AVMs
o Other vascular anomalies

4. CT Angiography (CTA) or MR Angiography (MRA)

• Non-invasive alternatives
• Increasingly used in acute settings for screening

Treatment of Aneurysmal SAH

Treatment focuses on:

1. Securing the aneurysm to prevent rebleeding:

o Neurosurgical clipping: open surgical approach
o Endovascular coiling: catheter-based approach (less invasive)
o Decision depends on aneurysm site, patient stability, and institutional expertise
2. Preventing and treating complications:
o Nimodipine for vasospasm
o Ventricular drainage for hydrocephalus
o ICU monitoring for early detection of vasospasm, seizures, and metabolic complications
3. Rehabilitation and follow-up:
o Many survivors require cognitive and physical rehabilitation
o Risk of rebleeding or new aneurysm formation persists in some patients
Arteriovenous Malformations (AVMs)

AVMs are congenital abnormalities consisting of abnormal tangles of arteries and veins with no intervening capillary bed.

Pathophysiology:

• High-pressure arterial blood is shunted directly into veins

• Causes venous hypertension, steal phenomena, and risk of hemorrhage

Clinical Features:

• Seizures
• Headaches
• Focal neurological deficits
• Intracerebral hemorrhage or subarachnoid hemorrhage, especially in younger patients

Diagnosis:

• CT or MRI: reveals serpiginous flow voids, hemorrhage

• Angiography: defines the feeding arteries, nidus, and draining veins

Treatment:

• Surgical resection (for accessible AVMs)

• Endovascular embolization
• Stereotactic radiosurgery for small, deep lesions
• Treatment decisions depend on size, location, and hemorrhage history
VASCULAR DISEASES OF THE BRAIN

(Part 6: Diagnostic Imaging, Acute Management, and Secondary Prevention of Stroke)

Imaging in Cerebrovascular Disease

Imaging plays a pivotal role in the diagnosis, management, and prognostication of cerebrovascular disease. The type and timing
of imaging are critical in both the acute and chronic stages.

1. CT Scan (Non-contrast)

A non-contrast computed tomography (CT) scan of the head is the first-line investigation in any suspected case of stroke
because it is:

• Fast
• Widely available
• Highly sensitive for detecting intracerebral hemorrhage (within minutes of onset)

In cases of ischemic stroke, CT may initially appear normal within the first few hours. However, signs of early infarction may
include:

• Loss of gray–white matter differentiation

• Sulcal effacement
• Hypoattenuation in a vascular territory
• Dense artery sign, indicating acute thrombus (e.g., dense MCA sign)

Serial CTs may later show cerebral edema, mass effect, or hemorrhagic transformation.

2. CT Angiography (CTA)

• Useful in visualizing large vessel occlusion, vascular anatomy, and identifying stenosis or dissection
• Often performed acutely in centers offering thrombectomy
• Can detect aneurysms or AVMs in cases of hemorrhage

3. MRI and MR Angiography (MRA)

MRI is more sensitive than CT for detecting early ischemic changes, particularly in:

• Brainstem
• Cerebellum
• Lacunar infarcts

Diffusion-weighted imaging (DWI) is particularly useful for identifying acute infarction within minutes of symptom onset.

MR Angiography (MRA) can evaluate arterial patency, collateral flow, and detect vascular malformations, often without
contrast.
4. Carotid Doppler Ultrasound

• Non-invasive method for assessing extracranial carotid stenosis

• Used in stroke risk assessment
• May reveal plaque ulceration, high-grade stenosis, or occlusion
• Commonly used to evaluate candidacy for carotid endarterectomy

5. Digital Subtraction Angiography (DSA)

• Remains the gold standard for detailed assessment of:

o Aneurysms
o AVMs
o Intracranial stenosis
• Used primarily when interventional treatment is planned

Acute Management of Stroke

The cornerstone of stroke treatment is rapid diagnosis and immediate intervention, ideally in a specialized stroke unit. The
goals are:

• Restore or preserve cerebral perfusion

• Prevent secondary injury
• Manage complications

Acute Ischemic Stroke

1. Thrombolysis (Alteplase – tPA)

• Indicated within 4.5 hours of symptom onset

• Requires no evidence of hemorrhage on CT
• Contraindications include:
o Recent surgery
o Active bleeding
o Very high BP
o Coagulopathy

Complication: intracerebral hemorrhage, hence strict selection criteria are essential

2. Mechanical Thrombectomy

• For large vessel occlusions (e.g., MCA, ICA, basilar artery)

• Can be done up to 24 hours in selected cases, especially with CT perfusion imaging
• Performed via catheter-directed clot retrieval

3. Supportive Measures

• Airway protection
• Maintain oxygenation and normoglycemia
• Control blood pressure cautiously
o Avoid aggressive lowering in acute ischemic stroke unless:
§ Systolic BP >220 mmHg
§ 185 mmHg if candidate for thrombolysis
• Avoid fever, treat infection aggressively
• Aspirin should be started after 24 hours if thrombolysis was used (immediately if not)
Intracerebral Hemorrhage

Management Priorities:

• Stabilize airway and vital signs

• Reverse anticoagulation if applicable (vitamin K, prothrombin complex)
• Control hypertension
o Rapid lowering of systolic BP to 140 mmHg is recommended unless contraindicated
• Monitor for raised intracranial pressure
o Treat with head elevation, osmotic agents, or ventricular drainage
• Surgical evacuation considered for:
o Cerebellar hemorrhages causing brainstem compression or hydrocephalus
o Lobar hemorrhages near the surface with mass effect

Subarachnoid Hemorrhage

Acute Measures:

• Admit to neurosurgical or neurocritical care unit

• Manage airway and monitor neurological status
• Control BP to reduce rebleeding risk
• Prevent vasospasm with nimodipine
• Treat hydrocephalus with ventricular drainage
• Early intervention (clipping or coiling) to secure aneurysm

Secondary Prevention

After the acute event, secondary prevention aims to reduce the risk of recurrence, through medical, surgical, and lifestyle
strategies.

Antiplatelet Therapy

• Aspirin, clopidogrel, or aspirin + dipyridamole are used long-term

• Not used concurrently with anticoagulants

Anticoagulation

• For cardioembolic stroke (e.g. atrial fibrillation)

• Choices include:
o Warfarin
o DOACs (e.g., apixaban, rivaroxaban)
• Initiated several days after ischemic stroke (timing based on infarct size and hemorrhagic risk)

Carotid Endarterectomy

• Recommended for patients with:

o Recent non-disabling stroke or TIA
o Symptomatic carotid stenosis >70%
• Benefit greatest if surgery is performed within 2 weeks
Lifestyle and Risk Factor Modification

• Control blood pressure (primary goal)

• Statin therapy even if cholesterol is normal
• Diabetes control
• Smoking cessation
• Regular physical activity
• Weight reduction
• Dietary changes

Conclusion

Cerebrovascular diseases are diverse in their etiology, presentation, and prognosis, but share a common requirement: prompt
identification and management. Advances in neuroimaging, thrombolytic therapy, endovascular techniques, and specialized
stroke care have transformed outcomes in recent decades.

However, prevention remains paramount. Rigorous risk factor management, timely intervention in high-risk individuals, and
public awareness are central to reducing the burden of these life-altering disorders.

3. Brain Tumours (Intracranial Tumours)

➤ Incidence and Distribution

Primary brain tumours occur in approximately 6 persons per 100,000 per year. Although fewer patients with metastatic brain
tumours reach neurosurgical centers, their actual incidence is likely to equal or even surpass that of primary tumours.
Approximately 25% of all patients with malignancy develop central nervous system (CNS) metastases. Among primary brain
tumours, about 1 in every 12 occurs in children under the age of 15.

➤ Tumour Site Distribution

• In Adults:
The most common tumours include:
o Gliomas
o Metastases
o Meningiomas
These tend to arise predominantly in the supratentorial compartment.
• In Children:
A larger proportion of tumours are located in the infratentorial compartment, especially:
o Gliomas
o Medulloblastomas

➤ Pathological Classification Overview

Intracranial tumours are commonly described as either:

• "Benign" – which can still have serious effects due to intracranial space limitation. For example, a benign astrocytoma
may widely infiltrate brain tissue, preventing surgical removal or may reside in functionally critical areas that make
resection hazardous.
• "Malignant" – which are typically characterized by:
o Rapid growth
o Poor differentiation
o High cellularity
o Mitotic activity
o Necrosis
o Vascular proliferation
However, unlike systemic malignancies, extracranial metastasis from primary brain tumours is rare.
In 2000, the World Health Organization (WHO) proposed a classification system for intracranial tumours based on tissue of
origin, moving away from umbrella terms such as "glioma." For example:

• Glioblastoma (previously considered embryonal) is now recognized as of astrocytic origin.

➤ Types of Intracranial Tumours

A. Neuroepithelial Tumours

• Astrocytes → Astrocytoma
o Most common primary brain tumour.
o Divided into grades I–IV, reflecting the degree of malignancy.
o Grading is based on histological biopsy, which may not represent the entire tumour.
o Glioblastoma multiforme (grade IV):
§ The most malignant and most frequent subtype.
§ Infiltrates surrounding tissues extensively.
§ High recurrence and poor prognosis.
o Other types:
§ Low-grade astrocytomas:
§ Includes:
§ Pilocytic (Grade I) – found in children and young adults, particularly:
§ Hypothalamic region
§ Optic nerve (especially with Neurofibromatosis type 1)
§ Cerebellum and brainstem
§ Diffuse types (Grade II):
§ Fibrillary
§ Protoplasmic
§ Gemistocytic
§ Often associated with p53 gene loss.
§ Characteristics:
§ Diffuse, slow-growing
§ No capsule or defined edge
§ Infiltrate surrounding brain tissue
§ Despite benign histology, often not curable due to invasive spread
§ Anaplastic astrocytoma (Grade III) and Glioblastoma multiforme (Grade IV):
§ Together form around 20% of primary intracranial tumours
§ Glioblastoma multiforme is more common than anaplastic astrocytoma
§ Median age of diagnosis:
§ Glioblastoma: 64 years
§ Anaplastic astrocytoma: 45 years
§ Rapid growth with widespread tissue invasion
§ Histology often reveals necrosis, cellular pleomorphism, and vascular proliferation
• Oligodendrocytes → Oligodendroglioma
o Typically slow-growing, well-defined tumours (Grade II).
o May appear with or without calcification.
o Variants include:
§ Anaplastic oligodendroglioma (Grade III)
§ Mixed oligoastrocytoma (Grade II) – composed of both astrocytic and oligodendroglial components
BRAIN TUMOURS

(Part 2: Ependymomas, Medulloblastomas, and Non-Neuroepithelial Tumours)

Ependymomas

Ependymomas arise from ependymal cells lining the ventricles and central canal of the spinal cord. In children, these tumours
most often originate from the floor of the fourth ventricle, where they may obstruct CSF outflow, leading to hydrocephalus. In
adults, ependymomas more commonly occur in the spinal canal.

Histological Features:

• Characteristically show perivascular pseudorosettes

• Can also show true ependymal rosettes
• Varying degrees of differentiation:
o Well-differentiated (Grade II)
o Anaplastic ependymomas (Grade III)

These tumours spread via cerebrospinal fluid pathways, and drop metastases can occur, particularly in anaplastic variants,
necessitating craniospinal imaging.

Medulloblastomas

Medulloblastomas are primitive neuroectodermal tumours (PNETs), typically located in the cerebellar vermis and found
almost exclusively in children.

Clinical Features:

• Raised intracranial pressure (due to obstructive hydrocephalus)

• Ataxia, especially truncal
• Nystagmus
• Morning vomiting and headache are common early signs

Histological Grade and Behaviour:

• Medulloblastomas are malignant (WHO Grade IV)

• Highly cellular with mitotic figures, necrosis, and neuronal markers
• Despite being malignant, they are radiosensitive and often respond to surgical resection + radiotherapy
• However, due to CSF dissemination, craniospinal radiotherapy is often necessary

Other Embryonal and PNET Tumours

Apart from medulloblastomas, supratentorial PNETs may arise in young children, presenting with:

• Seizures
• Hemiparesis
• Rapidly enlarging head circumference
• Signs of raised ICP

These are high-grade tumours, histologically resembling medulloblastomas, but located in the cerebral hemispheres.
Choroid Plexus Tumours

These rare tumours arise from the choroid plexus epithelium, more frequently in children, especially infants.

Types:

• Choroid plexus papilloma (benign)

o Most often in the lateral ventricle
o May cause hydrocephalus by overproducing CSF or blocking CSF flow
• Choroid plexus carcinoma (malignant)
o Aggressive with potential for CSF dissemination

Pineal Region Tumours

Tumours of the pineal gland region may include:

• Pineocytomas (well-differentiated)
• Pineoblastomas (high-grade, aggressive)
• Germinomas, particularly in young males

These may lead to:

• Parinaud’s syndrome: vertical gaze palsy

• Obstructive hydrocephalus due to aqueduct compression

Diagnosis often requires MRI and serum/CSF tumour markers, especially for germ cell tumours.

Craniopharyngiomas

Derived from Rathke’s pouch remnants, craniopharyngiomas are benign epithelial tumours usually found in the suprasellar
region. Most commonly seen in children and young adults.

Clinical Features:

• Bitemporal hemianopia from optic chiasm compression

• Growth retardation or delayed puberty
• Hydrocephalus
• Diabetes insipidus or other pituitary hormone deficiencies

Imaging Features:

• Frequently calcified
• Have both solid and cystic components
• May cause significant mass effect despite benign histology

Surgical resection is standard, but recurrence is frequent. Radiotherapy may be needed postoperatively.
Meningiomas

Arise from arachnoid cap cells, often at dural reflections, and are more common in middle-aged to elderly women.

Typical Locations:

• Parasagittal region
• Falx cerebri
• Convexities
• Sphenoid wing
• Olfactory groove

Characteristics:

• Usually benign and well-circumscribed

• Often calcified
• Hyperostosis of adjacent skull may be present
• May cause symptoms by compressing brain, not by invasion

Histological Subtypes:

• Transitional
• Fibrous
• Psammomatous (with psammoma bodies)
• Atypical or anaplastic (rare, more aggressive)

Meningiomas are often resectable, and many are incidental findings on imaging. Radiotherapy is used when surgery is
contraindicated or for residual/recurrent tumours.

BRAIN TUMOURS

(Part 3: Pituitary Tumours, Schwannomas, Lymphomas, Metastases, and Paraneoplastic Syndromes)

Pituitary Tumours

Most pituitary tumours are adenomas, arising from the anterior pituitary (adenohypophysis). They account for a significant
portion of intracranial neoplasms and may be either:

• Functioning (secretory), producing endocrine effects, or

• Non-functioning, presenting via mass effect

Clinical Features:

1. Endocrine Effects:
o Prolactinomas (most common):
§ Cause amenorrhoea, galactorrhoea, infertility, and hypogonadism
o Growth hormone-secreting adenomas:
§ Cause acromegaly or gigantism (if onset is pre-pubertal)
o ACTH-secreting adenomas:
§ Lead to Cushing’s disease
o TSH-producing adenomas (rare):
§ Cause hyperthyroidism
2. Mass Effect:
o Bitemporal hemianopia due to optic chiasm compression
o Headache
o If large enough, may cause hypopituitarism due to compression of normal gland
Imaging and Management:

• MRI is the modality of choice

• Microadenomas are <1 cm, macroadenomas >1 cm
• Medical therapy:
o Dopamine agonists (e.g. cabergoline) for prolactinomas
• Surgery:
o Trans-sphenoidal resection is the approach of choice
• Radiotherapy:
o Used for residual or recurrent tumours

Schwannomas (Vestibular and Others)

Schwannomas are benign tumours of the Schwann cells that form the myelin sheath of peripheral nerves. Within the cranial
cavity, they most commonly affect cranial nerve VIII (vestibulocochlear nerve), where they are referred to as vestibular
schwannomas or acoustic neuromas.

Clinical Features of Vestibular Schwannoma:

• Unilateral sensorineural hearing loss (most common initial symptom)

• Tinnitus
• Unsteadiness or imbalance
• Facial numbness or weakness (compression of adjacent cranial nerve V or VII)
• If large, may compress the brainstem or lead to hydrocephalus

Imaging and Management:

• MRI with gadolinium shows a mass at the cerebellopontine angle, often extending into the internal auditory canal
• Treatment options:
o Observation (small, slow-growing tumours)
o Microsurgical removal
o Stereotactic radiosurgery

Vestibular schwannomas may be bilateral in Neurofibromatosis Type 2 (NF2), a key diagnostic criterion for this genetic
condition.

Central Nervous System Lymphoma

Primary CNS lymphoma (PCNSL) is a high-grade B-cell lymphoma, often diffuse large-cell type, that arises within the brain,
leptomeninges, eyes, or spinal cord, without systemic lymphoma.

Risk Groups:

• Immunocompromised individuals, especially those with HIV/AIDS

• Increasingly seen in immunocompetent elderly patients

Clinical Features:

• Focal neurological deficits

• Cognitive changes
• Seizures
• Headache
• Visual disturbances if ocular involvement
Imaging:

• MRI shows homogeneously enhancing lesions, often periventricular

• May be multiple or solitary
• Lesions may involve deep structures (e.g. basal ganglia, corpus callosum)

Management:

• High-dose methotrexate-based chemotherapy is mainstay

• Steroids can shrink lesions but may obscure diagnosis if biopsy delayed
• Radiotherapy is used in selected cases but may worsen cognitive decline in older adults

Metastatic Brain Tumours

Metastases to the brain are more common than primary brain tumours, particularly in adults. About 25% of patients with
systemic cancer will develop brain metastases.

Common Primary Sources:

• Lung
• Breast
• Melanoma
• Renal cell carcinoma
• Colorectal carcinoma

Typical Features:

• Multiple lesions are more common than solitary

• Occur at gray-white matter junctions
• Produce symptoms of raised intracranial pressure, seizures, or focal deficits

Imaging:

• MRI with contrast is the most sensitive

• Lesions are often ring-enhancing and surrounded by vasogenic edema

Management:

• Corticosteroids to reduce edema

• Whole-brain radiotherapy
• Stereotactic radiosurgery for selected lesions
• Surgical excision for solitary accessible metastases
• Systemic treatment of the primary malignancy

Paraneoplastic Syndromes Affecting the CNS

Paraneoplastic neurological syndromes are autoimmune-mediated neurological disorders triggered by a remote malignancy,
without direct invasion or metastasis.

Mechanism:

• Tumour antigens resemble neuronal antigens

• Leads to immune cross-reactivity against the CNS or peripheral nervous system
Examples:

• Subacute cerebellar degeneration: ataxia, nystagmus, dysarthria

o Associated with breast, ovarian, lung cancers
• Limbic encephalitis: memory loss, seizures, behavioural changes
• Paraneoplastic opsoclonus-myoclonus
• Stiff-person syndrome
• Sensory neuronopathy (dorsal root ganglionopathy)

Diagnosis:

• Often clinical, supported by antibodies (e.g., anti-Hu, anti-Yo, anti-Ri)

• MRI may show temporal lobe or cerebellar abnormalities
• CSF may show inflammatory changes

Management:

• Identification and treatment of the underlying tumour

• Immunotherapy: steroids, IVIG, plasmapheresis
• Often irreversible if delayed

HYDROCEPHALUS

Definition

Hydrocephalus is defined as an active dilatation of the brain’s ventricular system resulting from an imbalance between
cerebrospinal fluid (CSF) production and absorption. This excludes ventricular enlargement secondary to brain atrophy, which
is classified separately as hydrocephalus ex vacuo.

CSF Formation and Flow

CSF is produced at an approximate rate of 500 ml/day (0.35 ml/min), primarily by the choroid plexus located within the lateral,
third, and fourth ventricles. From there, it flows in a caudal direction through the ventricular system:

• Lateral ventricles → Foramen of Monro → Third ventricle → Aqueduct of Sylvius → Fourth ventricle
• CSF exits the fourth ventricle via the foramina of Luschka and Magendie into the subarachnoid space, passing through
the tentorial hiatus to reach the cerebral convexities
• Absorption occurs through arachnoid granulations into the venous system

Classification

Hydrocephalus is divided into:

1. Obstructive (Non-communicating):
o Obstruction occurs within the ventricular system
o CSF does not communicate freely with the subarachnoid space
2. Communicating:
o Obstruction occurs outside the ventricular system, often in the arachnoid villi
o Ventricular system remains in continuity with subarachnoid space

Causes of Hydrocephalus
Obstructive Hydrocephalus

• Acquired:
o Aqueductal stenosis (infection or haemorrhage)
o Mass effect (supratentorial tumours)
o Intraventricular haemorrhage
o Tumours (colloid cysts, pineal masses, posterior fossa lesions)
o Abscesses or granulomas
o Arachnoid cysts
• Congenital:
o Aqueductal forking or stenosis
o Dandy–Walker syndrome (atresia of foramina of Luschka and Magendie)
o Chiari malformation

Communicating Hydrocephalus

• Infections (pyogenic, TB, fungal)

• Subarachnoid haemorrhage (spontaneous, traumatic, post-operative)
• Carcinomatous meningitis
• Increased CSF viscosity (e.g. high protein)
• Overproduction of CSF (e.g. choroid plexus papilloma)

Pathological Effects

• In infants, before fusion of cranial sutures:

o Leads to massive head enlargement, with thinning of cerebral mantle
o May result in death if untreated, although arrested hydrocephalus may occur where ventricles remain dilated
but pressure normalizes
• In older children/adults, ventricular enlargement can cause:
o Increased intracranial pressure (ICP)
o White matter damage
o Periventricular gliotic scarring
o Some CSF absorption may occur via periventricular blood vessels

Clinical Features

Infants and Young Children

• Bulging anterior fontanelle

• Dilated scalp veins, thin scalp
• ‘Cracked pot’ percussion sound over skull
• Increased head circumference (compare with growth charts)
• Setting-sun sign: impaired upward gaze
• Vomiting, irritability, drowsiness
• Failure to thrive or mental retardation in slow-onset cases

Juvenile/Adult Hydrocephalus

• Acute onset: headache, vomiting, papilloedema, impaired upward gaze, rapid decline in consciousness
• Gradual onset:
o Dementia
o Gait ataxia
o Urinary incontinence
o This triad may occur even if CSF pressure appears normal: Normal Pressure Hydrocephalus (NPH)
Investigations

Imaging

• Ultrasound (via anterior fontanelle in infants) for ventricular size

• CT/MRI:
o Shows ventricular dilation
o Detects periventricular lucency, masses, or CSF obstruction
o Assesses whether 4th ventricle is dilated or compressed:
§ Dilated 3rd and lateral ventricles + normal 4th: aqueductal stenosis
§ Global dilation: communicating hydrocephalus
§ Deviation or compression of 4th ventricle: posterior fossa mass

Other Tools

• ICP monitoring in suspected NPH

• Developmental and psychometric assessments in children for baseline comparison

Normal Pressure Hydrocephalus (NPH)

Defined by the clinical triad of:

• Gait disturbance
• Dementia
• Urinary incontinence

Despite normal CSF pressure, ventricular enlargement leads to:

• Frontal lobe pressure → dementia

• Paracentral lobe pressure → incontinence
• Stretching of leg fibres/internal capsule → gait abnormalities

May follow trauma, meningitis, SAH, radiation, or be idiopathic. Diagnosis is based on clinical features and MRI/CT evidence.
CSF shunting may help in up to 70% of cases with a preceding cause

Management of Hydrocephalus

Acute or Progressive Hydrocephalus

• Ventriculoperitoneal (VP) shunt

• 3rd ventriculostomy (especially if triventricular)
• Lumbar puncture (if communicating hydrocephalus e.g. post-SAH)
• Removal of mass lesion if obstructing

Chronic or Stable

• “Arrested hydrocephalus”: no treatment unless developmental concerns arise

Shunt Systems and Complications

 • Shunts may include valves (fixed, flow-regulated, or programmable)
• Lumboperitoneal shunts may be used in communicating hydrocephalus
• Reservoirs allow aspiration of CSF if needed

Complications:

• Infection (e.g., Staph. epidermidis, Staph. aureus): meningitis, peritonitis, nephritis (especially with V-A shunts)
• Shunt obstruction: due to clot, debris, omentum, or tumour; confirmed via imaging
• Subdural hematoma: from brain collapse and vein tearing; mitigated with programmable valves
• Low pressure syndrome: postural headaches; may require high-pressure valve or anti-siphon device

OSTEOARTHRITIS OF THE SPINE

(Cervical Spondylosis and Lumbar Degenerative Changes)

Cervical Spondylosis – Overview and Pathogenesis

Cervical spondylosis refers to the degenerative osteoarthritic changes that affect the cervical spine, particularly prevalent in
individuals over the age of 50. More than half of this population exhibit radiographic signs of spondylosis, although only about
20% develop clinical symptoms. Surgical treatment is rarely required.

The cervical spine, due to its mobility and mechanical stress, is particularly prone to degenerative transformation. The
pathological cascade usually begins with degeneration of the intervertebral discs, which results in:

• Disc collapse
• Formation of osteophytes (bony outgrowths)
• Protrusion of the annulus fibrosus
• Hypertrophy of the apophyseal (facet) joints
• Thickening of the ligamentum flavum
• Instability between vertebral bodies

These changes progressively reduce the diameter of the spinal canal and intervertebral foramina, leading to spinal cord and/or
nerve root compression.
Clinical Manifestations of Cervical Spondylosis

The clinical effects are divided into two primary syndromes:

1. Cervical Radiculopathy

This occurs due to compression of the spinal nerve roots exiting the cervical spine, commonly affecting levels C5 to C8. The
clinical signs may involve both sensory and motor dysfunction, following the specific dermatomal and myotomal distributions of
the affected root.

Symptoms:

• Pain: sharp, stabbing pain, worse on coughing or sneezing; may radiate over the shoulders, down the arms, or into the
scapular region
• Paraesthesia: tingling, numbness in a dermatomal distribution
• Muscle weakness in specific groups, e.g.:
o C5–C6: deltoid, biceps
o C7: triceps
• Reflex impairment:
o C5–C6: diminished biceps and supinator jerk
o C7: diminished triceps jerk
• Trophic skin changes: dry, blue, cold, and scaly skin over the affected area in longstanding compression

2. Cervical Myelopathy

This syndrome arises from direct compression of the spinal cord within the narrowed canal. Involvement of vascular elements
may exacerbate the damage. Trauma may trigger symptom progression or be absent entirely.

Clinical Signs:

• Gait disturbance, clumsiness of hands

• Lower motor neuron (LMN) signs in upper limbs: wasting, weakness, hyporeflexia
• Upper motor neuron (UMN) signs in lower limbs: spasticity, hyperreflexia, Babinski sign
• Bladder dysfunction in severe cases

Investigations

• Plain X-rays of the cervical spine:

o Assess loss of normal cervical lordosis
o Look for disc space narrowing, osteophyte formation
o Foraminal narrowing is best seen in oblique views
o Flexion/extension views may assess instability or subluxation
• MRI (preferred):
o Sagittal views visualize the full spinal cord
o Hyperintensity on T2-weighted images suggests spinal cord edema/damage
o Axial views show precise root compression and foraminal encroachment
• CT myelography:
o Useful in patients with MRI contraindications
o Details osteophytic compression and root narrowing

Management of Cervical Spondylosis

Conservative Treatment

• Analgesics and anti-inflammatory agents

• Cervical collars for short-term support
• Physiotherapy
• Most cases of radiculopathy respond to non-operative management and reassurance

Surgical Treatment

Indicated in:

• Progressive neurological deficit

• Disabling myelopathy
• Severe, refractory radicular pain

Surgical Options:

1. Anterior approach (ideal for focal disc protrusion at 1–2 levels):

o Discectomy and fusion
o Prosthetic disc replacement or bone graft
2. Posterior approach (multilevel disease or congenital canal stenosis):
o Laminectomy (C3–C7)
o Foraminotomy for root decompression at specific levels

Modern surgeries may involve interspinous distractor implants, although these remain under evaluation.

INJURIES OF THE SPINE AND SPINAL CORD

Epidemiology and General Considerations

Each year, approximately 2 per 100,000 people experience a spinal injury, with half of these involving the cervical region. At
the moment of impact, there may or may not be direct damage to the spinal cord itself. However, post-traumatic spinal
stability is critically important — as instability at the injury site may later result in worsening cord injury during transportation
or clinical handling.

Mechanisms of Spinal Injury

The mechanism of injury largely determines whether the injury is stable or unstable, and influences treatment decisions.

Mechanisms Include:

• Vertical Compression:
o Occurs when an object falls onto the head, or from a jump/fall from height
o Leads to burst fractures or anterior wedge collapse
• Hinge Injury:
o Often caused by backward flexion (e.g., blow to the forehead or weight falling on the back)
o May result in hyperextension injuries with rupture of the anterior longitudinal ligament
• Shearing Injury:
o Involves a combination of rotational and axial forces (e.g., road traffic accident)
o Often leads to dislocation or fracture-dislocation with ligament disruption
• Flexion/Extension with Ligamentous Damage:
o May produce instability without fracture, especially in the cervical spine due to horizontal facet orientation
Initial Clinical Assessment

Spinal injury should always be suspected in trauma patients, particularly if:

• They are unconscious, or

• There is pain, weakness, numbness, or incontinence

Signs Suggestive of Spinal Cord Injury:

• Bilateral flaccid limbs

• Absent limb reflexes
• Unresponsiveness to painful stimuli
• Painless urinary retention
• Priapism
• Neurogenic paradoxical ventilation (chest indrawing during inspiration due to absent intercostal muscle function in
cervical cord lesions)

Visible deformities include gaps between spinous processes or paraspinal swelling, suggestive of interspinous ligament rupture.

Radiological Evaluation

Plain X-rays:

• Lateral views must include C6–C7, and show:

o Soft tissue swelling
o Loss of vertebral alignment
o Disc space widening
o Subluxations
o ‘Burst’ fractures or wedge compression
• AP and Oblique Views:
o Assess alignment of spinous processes and facet joints
o Oblique views help assess foramina narrowing
• Open mouth view (odontoid view):
o Demonstrates C1–C2 integrity
o >7 mm offset between lateral masses of C1 over C2 indicates transverse ligament disruption (Spence’s Rule)

CT and MRI:

• CT: excellent for assessing fracture lines, especially in axial and sagittal reconstructions
• MRI: useful for soft tissue, disc herniation, or epidural haematoma, although it rarely alters acute management

Spinal Injury Types and Treatment by Region

CERVICAL SPINE

Stable Injuries:

• E.g. anterior wedge, hyperextension

• Managed conservatively with a cervical collar

Unstable Injuries:
 • May require 12 weeks of skull traction, Halo vest, or operative fixation
• Persistent instability requires surgical fusion

Odontoid Fractures (C2):

• Require rigid immobilisation (e.g., Halo)

• If union fails: posterior C1–C2 fusion

THORACIC SPINE

Stable Fractures:

• E.g. wedge compression

• Managed with analgesia and resumption of activity once pain subsides

Unstable Fractures/Dislocations:

• Typically result from high-impact trauma

• If no cord damage: managed conservatively
• Surgical fixation increasingly preferred to allow early mobilisation

THORACOLUMBAR SPINE

Stable Fractures:

• E.g. wedge or burst fractures

• Treated with mobilisation ± supportive brace

Unstable Fractures or Dislocations:

• Require operative fixation

• Techniques include:
o Anterior and/or posterior reduction
o Screw-rod systems
o Hartshill rectangle constructs
• Without cord damage: supportive braces may suffice
• With paraplegia: conservative treatment, including bed rest in a plaster jacket, although this risks pressure sores

Management Principles

• Unstable injuries must be immobilised or fixed surgically to prevent cord compression

• Surgical decompression of the spinal cord is generally not shown to improve neurological outcomes, unless there is:
o Progressive deterioration in incomplete cord injuries
• Steroids (e.g. methylprednisolone) were historically considered beneficial if given within 8 hours, but later analysis
raised concerns about infection risk and methodological flaws — use is now debated

Paraplegia and Rehabilitation

Once spinal cord injury is established, rehabilitation begins. Early transfer to a specialised spinal injury centre ensures optimal
recovery.

1. Skin Care:

• Turn every 2 hours to prevent pressure sores

• Avoid friction or contact with bony prominences
• Air/water beds or sheepskin overlays may assist

2. Urinary Tract:

• Long-term management includes:

o Indwelling catheters
o Intermittent catheterisation
o Reflex bladder training (cord lesion)
o Abdominal compression voiding (root lesion)
o Bladder neck surgery if needed

3. Limb Management:

• Physiotherapy prevents contractures and improves functional mobility

• Spasticity, flexor spasms, and reflex bladder may develop

Prognosis Based on Lesion Level

High Cervical Lesions (Above C4):

• Often fatal without ventilatory support

• Those who survive may be totally dependent

Sparing of C7 Segment:

• Preserves elbow and wrist extension

• Enables some independence (e.g., transfer from bed to wheelchair)

Thoracolumbar Lesions:

• Generally, good prognosis

• Most patients regain independence

Mixed Cord and Root Lesions (e.g., at L1):

• Roots are more resistant to injury ("root escape")

• Recovery is possible over months
• Motor limbs remain flaccid, but function may slowly return