CASE 6 REVISION – COGNITIVE IMPAIRMENT

“HIGH LEVEL” LEARNING OUTCOMES NEUROANATOMY OF THE BRAIN (L) - GENERAL

 Describe the functional anatomy of the brain - the main The brain is composed of the
regions of the brain, their blood supply and cerebrum, cerebellum and brainstem.
 function. There are 3 poles: frontal, occipital and
 Relate the main structures of the brain to their radiological temporal.
images on CT scan and MRI
 Describe structure and function of the hearing apparatus Gyrus’ are ridges and sulcus’ are
 Identify the different cell types present in the brain and grooves/dips.
their role in injury and repair Nuclei are collections of cell bodies in
 Outline synaptic transmission in the brain the CNS, and ganglia are cell bodies in
 Describe how memories are stored in the brain and the the PNS.
neural networks underpinning cognitive function. White matter is found in the centre of the brain and is stained black by
 Discuss the determinants of cognitive health over the life Weigerts stain which stains myelin. It in a connection area made of glial
course cells and myelinated neurones. Grey matter is found in cortex and is
 Describe changes in brain structure and cognitive function unstained. It is involved with cognition and higher functions.
across the life course
 Discuss societal attitudes and predominant preconceptions
with respect to sensory impairment, ageing
NEUROANATOMY OF THE BRAIN (L) - BRAINSTEM
 and older people The BRAINSTEM is composed of the midbrain, pons and medulla
 Describe the psychological impact of ageing and cognitive oblongata (from top to bottom). 10 of the 12 cranial nerves arise from the
change on individuals and families brainstem and supply sensory and motor innerv to face and neck.
 Describe the functional anatomy of the inner ear
There are 3 main tracts running through
 Explain the different mechanisms of hearing loss
the brainstem to the body:
 Discuss the role of non-governmental organisations in
Corticospinal/pyramidal
supporting patients with specific age related
motor; has axons from motor
 conditions
cortex, there are 2 tracts: anterior
 Describe the role of carers in community based support
and lateral. They decussate in the
medulla which is why one side of
NEUROANATOMY OF THE BRAIN (L) - CEREBELLUM brain controls opp side of body. The lateral
Main function is in motor control. It corticospinal tract is made of the fibres that
doesn’t initiate action but rather fine decussate in medulla; it leaves anterior horn of
tunes it, and is involved in control/ SC and controls limbs. Anterior corticospinal controls axial muscles.
planning and precision of movement. Spinothalmic – originates in spinal cord and sends info about pain to
It is also involved in balance and muscle thalmus. Lateral tract = pain and temp, anterior = crude touch & pressure
tone. May be involved with attention and Posterior column-medial lemniscus pathway – fine touch, vibration and 2
language. point discrimination. Posterior tract in the spinal cord and medial
It lies behind the brainstem and below the cerebrum, but has leminiscus to the brainstem. Some synapse in medulla (medial
lots of connections with both. leminiscus) others in thalmus (posterior?).
The midbrain controls vision, hearing, temperature, sleep/awake and
NEUROANATOMY OF THE BRAIN (L) – SULCUS’ motor control. Dopamine is produced here by substantia nigra. Sits on the
tectum and has anteriorly, the cerebral peduncles, & posterior – colliculi.
The longitudinal fissure separates the two hemispheres of the The pons links medulla and midbrain. Contains pneumotaxic centre
brain. The corpus callosum runs below the longitudinal fissure (controlling insp and exp). CNs 5,6,7 and 8 arise here. Controls resp,
and cerebral cortex. The falx cerebri (dura mater) runs in this sleeping, bladder, taste, hearing and loads of other shit.
groove also. The medulla also controls some ANS functions (it contains the resp, cardio
Central sulcus – separates and vomiting centres) and so controls BP, breathing and HR).
the frontal and parietal The midbrain connects the brainstem to the hemisphere. The brainstem
lobes. passes out of the foramen magnum to become the spinal cord.
Lateral sulcus (Sylvian
fissure) – separates the
frontal and occipital lobes.
NEUROANATOMY OF THE BRAIN (L) – CORPUS CALLOSUM
Parietal-occipital sulcus – separates The corpus callosum connects the L+R cerebral
the parietal and occipital lobes. hemispheres and ensures they don’t act
independently. It is a band of white matter.
The anterior commissure is part of the corpus
NEUROANATOMY OF THE BRAIN (L) – DIENCEPHALON callosum that connects the temporal lobes.
Consists of the thalmus (2x thalami), hypothalamus and pineal
gland. It sits on top of the midbrain.
It projects fibres into the cerebral cortex, and also receives
them from the cortex. Acts as a gateway.
Thalmus processes and relays sensory info
(incl. pain) and is involved in
wakefulness.
Hypothalmus links the nervous and The anterior commissure and the
endocrine systems via pituitary. corpus callosum together are
Controls temp, sleep, thirst and called the inter-hemispheric
circadian rhythms. Also secretes hormones. commissures.
Pineal gland produces melatonin from
serotonin involved in circadian rhythms and Splenium is swollen because
sleep patterns. visual cortex is in occipital lobe.
 CASE 6 REVISION – COGNITIVE IMPAIRMENT

NEUROANATOMY OF THE BRAIN (L) - VENTRICLES NEUROANATOMY OF THE BRAIN (L) – CIRCLE OF WILLIS
 There are 4 ventricles filled with CSF produced by the The blood supply of the brain is via the
choroid plexus’ in the lateral ventricle. internal carotid and vertebral arteries
 The CSF is reabsorbed into the venous system. which unite to form the
 There are 2 lateral ventricles and 1 of each of the others. basillar artery.
 After the fourth ventricle the CSF enters the sub-arachnoid The A+P comm supply the
space thalamus and basal ganglia.
 The lateral ventricle has an The vertebral arteries
anterior (frontal lobe), supply the medulla.
inferior (temporal lobe) and Branches of the basilar supply the
posterior horn (occipital cerebelum and pons.
lobe).
 Inside = ependyma epi cells The anterior cerebral supplies the frontal
lobes and medial aspects of parietal
and occipital.
The middle cerebral supplies the temporal
lobe and motor cortex.
The posterior cerebral supplies the
occipital lobe and
hippocampus.
The middle,
vertebral and
basilar arteries
aren’t considered
NEUROANATOMY OF THE BRAIN (L) part of the Circle of Willis.
- INSULA
Sunken part of
cerebral cortex
that lies in the
lateral sulcus.
It has autonomic
effects and
controls emotions etc?
Also consciousness,
self awareness etc. NEUROANATOMY OF THE BRAIN (L) – CEREBRAL HEMISPHERES
Responsible for higher functions. Consists of an outer cortex which is
NEUROANATOMY OF THE BRAIN (L) – INTERNAL made up of 6 layers of grey matter, and an inner medulla which is made
Contained in the cerebral hemispheres are the basal ganglia, up of white matter.
limbic system and ventricles. Cortex
The basal ganglia are cell bodies contained in white matter. The areas of the cortex with 6 layers is called the neocortex (higher
Consists of: function; language and conscious thought); any fewer is called the
Note the hippocampus is in the
- Caudate nucleus temporal lobe and is connected to the allocortex.
- Putamen cerebrum by the fornix. It is involved LOBES
- Globus palidus Frontal lobe – decision making, problem solving and planning. Contains
in memory, endocrine control (hypoth)
- Substantia nigra motor cortex and involved in personality and higher emotions.
- Hypothalamic nucleus Parietal lobe – integrates sensory information.
The limbic system is involved Temporal lobe – memory, language, emotion, hearing and learning;
with emotion, behaviour, memory contains hippocampus.
and motivation, and consists Occipital lobe – visual cortex
of: Premotor cortex – frontal lobe; planning movement. MCA
- Hippocampus Primary motor cortex – frontal lobe; plan and execute movement. MCA
- Fornix Somatosensory cortex – parietal; sense of touch. MCA
- Mammillary bodies Broca’s area – frontal lobe; production of speech. MCA
- Amygdala (aggression and rage) Primary auditory cortex – temporal lobe; sense of hearing. MCA?
Primary visual cortex – occipital lobe; seeing stuff. PCA
Pre-frontal – frontal; executive function, social skills; personality. A+MCA.
Wernicke’s – temporal lobe; interpretation of speech. MCA.
Retrosplenial cortex – involved in
spatial awareness and
navigation
Hearing words = auditory
cortex, seeing words = visual
cortex, thinking about words =
prefrontal cortex and
speaking words: Broca’s area
Association areas are to
do with our perceptions &
how we integrate diff functions.
 CASE 6 REVISION – COGNITIVE IMPAIRMENT

NEUROANATOMY OF THE BRAIN (L) – CROSS SECTIONS NEUROANATOMY OF THE BRAIN (L) – TEMPORAL L .
Each temporal lobe is found
below each lateral sulcus.
Has structures such as
the hippocampus and
the amygdala which
are part of the limbic
system. They are
involved in long term
memory.
The superior
temporal gyrus has primary auditory cortex
and Wernicke’s area.
The inferior temporal gyrus is to do with vision, complex visual
objects and recognition of faces.

NEUROANATOMY/IMAGING OF THE BRAIN (L)

White matter is myelinated axons; it is arranged in tracts
(connecting 2 parts of the CNS) and fascicles.
The cortical medulla has axons going in and
out of brain.
 The CNS has no CT
 Synaptic transmission takes
place in nuclei in grey matter
 White matter (axons) connect
grey matter
(cell bodies)
 The cortex has 6 layers, but in
hippocampus has 3.
 There are 3 ways grey matter can
be arranged: arranged in nuclei, layers (laminae) or
reticular (found in brainstem; meshwork of nerves/fibres)
 Laminae (layers)can be connected by assoc fibres which
connect areas on same side or commissural fibres;
connect areas on opp sides
NEUROGLIAL CELLS
Non-neuronal cells that help maintain the NS. Many more than
neurones.
Oligodendrocytes
Myelinate the CNS neurones. They have 5 processes that
branch and surround multiple (15-25) neurones. They
establish nodes of ranvier. Myelination occurs post-natally.
Degenerate as get older, and in MS. Oligodendrogliomas
cause seizures due to damage in the CNS.
Astrocytes
Found throughout the CNS they are star shaped and form an
interconnected network. They can be visualised with antibody
GFAP (glial fibrillary acidic protein). They regulate Ca2+ that
must be kept under 100nM – this contraction and exocytosis
of NTs, but also gene expression and metabolism in CNS. A
There are 2 large bits of white matter: corpus callosum and the internal pair of astrocytes are coupled by 200 porous gap junctions.
capsule. This allows for diffusion of NTs, nucleotides and ions.
There are 3 large bits of grey matter: the amygdala, hippocampus and the Functions:
thalmus. 1. Blood brain barrier – form part of the blood brain barrier
and secrete vasodilator/constrictors to control BF to CNS
tissue
NEUROANATOMY OF THE BRAIN (L) 2. Extracellular K+ - absorb it and redistribute from
– INTERNAL CAPSULE exctracellular space. Poor function = epilepsy
3. Extracellular glutamate – has to be kept at 3mM because
Contains ascending and descending axons. it’s toxic to neurones
It separates the thalamus and caudate nucleus 4. Ca2+, Cl- and H20 conc – need to keep levels constant in
from lentiform N. Contains lots of tracts. extracellular space
It also contains the corticospinal tract. 5. Metabolic support – converts glucose to lactate which is
Carries info from primary motor cortex to released and taken up by neurones.
the spinal cord. 6. Control of breathing – sensitive to PH so if PH is low, they
cause an AP to increase RR.
Has three parts: the anterior limb, the genu Pathology: Astrocytomas are slow growing tumors that are
(formed of geniculate fibres that decussate and hard to detect and remove; astroglosis is isolation of a
end in cranial nerves) and the posterior limb. damaged area and rebuilding the BBB for new circuits.
 CASE 6 REVISION – COGNITIVE IMPAIRMENT

NEUROANATOMY/IMAGING OF THE BRAIN (L) CONT. THE BRAIN AS AN ORGAN (P)

Microglia The dura mater is a dense
Provide protection because the CNS cannot regenerate. They fibrous tissue that prevents
are the immune cells (equiv of macrophages) of the CNS that the brain from moving. The dura has
are activated by brain injury (e.g. hypoxia). 2 layers: an outer periosteal layer that
Ependymal cells adheres to the cranium, and an inner
Ciliated cuboidal epithelial cells that line the ventricles of the meningeal layer. The falx cerebri
brain. They are modified to produce CSF and form the choroid reflects away from periosteal layer in the
plexus’. They can form ependyomas (benign but occupy space). longitudinal fissure to separate the 2 cerebral hemispheres. The
tentorium cerebelli separates the occipital lobe from the cerebellum,
Neurotransmission and the falx cerebelli separates the two hemispheres of the cerebellum.
Neurones form a tripartite synapse which is formed by 2
astrocytes and a pre-synaptic neurone and the post-synaptic The space between the dura mater and the arachnoid mater is called
membrane. Astrocytes reg the activity of the neurone. the subdural space, and the space between arachnoid and pia is the
subarachnoid space. Infection of meninges causes meningitis.
Neurotransmitters
 The corpus callosum connects the L+R cerebral hemispheres; this
Excitatory NT = Glutamate: formed from glutamine in the
is called a commissure.
mitochondria of the pre-synaptic neurone by glutaminase
 On the base of the brain is the infundibulum which is an extension
enzyme. It is released via exocytosis where it is then
of the hypothalamus that connects the pituitary to the brain.
reabsorbed by astrocytes, converted to glutamine by glutamate
 The oculomotor nerve arises from the midbrain (3)
synthetase and taken up by the pre-synaptic neurone.
 Trigeminal N. from medulla (5)
Inhibitory NT = GABA: formed from glutamine in mitochonbdria  Vagus N. from pons (10)
by glutaminase, then by glutamic acid decarboxylase to GABA.  Foot movement is supplied by anterior cerebral artery
Then released by exocytosis where it’s reabsorbed by AT by  Hand movement by middle cerebral artery
astrocytes and the process is reversed where it is taken up by  Vision by posterior cerebral artery
pre-synaptic neurone as glutamine.  Sensation in toes – ACA
Cholinergic neurones – Ach is the NT for 2 groups of neurones  Hearing and smiling MCA
in the pons: subthalmic nucleus and substantia nigra  The two arteries supplying the brain are the internal common
(stereotyped movement) and forebrain cholinergic nuclei carotid and the vertebral arteries.
(memory).  The vertebral arteries fuse to form the basilar artery which overlies
Monoamine NTs the pons
Noradrenaline in lateral coeruleus which projects to rest of
brain and lateral tegmental which is involved in urinary Straight sinus Superior sagittal Venous drainage of the
continence. Lack in cortex can cause depression. sinus brain is via the internal
Dopamine in the substantia nigra where it’s implicated in jugular vein.
Parkinson’s and also if there’s too much or too little it can The dural venous sinus’
cause schizophrenia. Inferior sagittal drain the brain. The
Serotonin (5HT) – found only in the raphe nuclei of the sinus superior sagittal and
midbrain. It has a spinal projection which can cause analgesia straight sinus join at the
in dorsal horn and urinary continence. Rostral projection to confluence of sinus’.
cerebral cortex and hypothalamus is involved in sleep/wake Great cerebral vein
states and interacts with dopamine to cause schizophrenia.
Also implicated in SIDs. Great cerebral and inferior
Transverse
sagittal join to form the
sinus’
INSIDE THE BRAIN (P) straight sinus.
Cavernous
Note the genu and fornix – sinus
2 major areas of white
matter. OTHER ANATOMY
 The 3rd ventricle lies
in the midline in the Arachnoid granulations are bits of the arachnoid that protrude into the
cerebral hemispheres. meningeal layer of the dura mater, and thus into the dural venous
 The fourth ventricle sinuses and transfer CSF to the venous system.
lies posterior to the pons The nueorcranium forms the skull; it is made up of 8 bones: frontal,
and upper medulla ethamoid, sphenoid, occipital, parietal (x2) and temporal (x2).
 CSF is found in the subarachnoid space CNs 3, 4 all derive from the midbrain.
 Arachnoid granulations reabsorb CNS
into the dural venous sinus’, CNs 5 derive from the pons
especially the superior sagittal sinus. CN 8, 9, 10, 11 and 12
 The green area on the MRI is the arise from medulla.
hippocampus CNs 6 (abducens)
 The fornix transmits info from the and 7
rolled up cortical area called the (facial) arise from
hippocampus junction
 In the picture to the right, between pons
number 1 is hippocampus, and medulla.
2: caudate nucleus,
3: corpus callosum, There is also the
4: lateral ventricles, viscerocranium;
5: 3rd ventricle and 6 is the but that shit’s
interpenduncular cistern too hard. So
contains circle x wilis. deal with it.
 CASE 6 REVISION – COGNITIVE IMPAIRMENT

HEARING (L) THE INNER EAR (L)

Sound is the compression of air; the frequency of this ∞ Tonotopy is the frequency of sound causing it to travel different
compression that we interpret as sound is measure in lengths along the basillar membrane. It is the relationship between
Hz. position on the basillar membrane and differeing frequancies.
The human range of hearing is 20Hz to 20kHz, ∞ The lower the frequency the further it travels along the basillar memb
however this range decreases as we age ∞ Cochlea implants work on the principle of tonotopy – can be used in
(presbycusis), especially at higher frequancies. people with sensorineural hearing loss as long as they have a
Conductive hearing loss – occurs if the problem is in functioning cochlear nerve (i.e. the problem is with their hair cells)
the outer or middle ear. ∞ With implants a processer is inserted into the ear that breaks sound
Sensorineural hearing loss – occurs if the problem is down into its frequency components and then sends it to the basillar
in the cochlear (sensori) or the auditory N. (neural) membrane where particular parts are stimulated
Otosclerosis is the calcification of the joints between ∞ High freq sounds activate electrodes at base of cochlear, and low
the ossicles. This leads to reduced hearing acuity due freq activate electrodes at apex of cochlear
to decreased movement. Especially in the joint ∞ The primary auditory cortex is found in Heschel’s gyrus in temporal
between the stapes and round window. lobe; it has a tonic map of frequancy
Otitis media is a condition whereby ∞ Wernicke’s area is supplied by the middle cerebral artery and found
inflammation/infection leads to fluid build up in the in the temporal lobe. It is involved in interpretation of speech. With
middle ear. This can perf the ear drum, however Wernicke’s aphasia – you talk fluently but talk shit.
grommets allow fluid to drain naturally. ∞ Broca’s area is supplied by MCA and in temporal lobe. It is involved
The tectorial membrane doesn’t move; the basilar in producing speech so aphasia causes stilted speech with no
memb moves causing the hair cells to move across conjunctions/pronouns etc.
the tectorial membrane. ∞ Both Wernicke’s and Broca’s areas are in left (dominant hemisphere)
Endolymph – found in scala media (cochlear tube). It and surround primary aud cortex. They make up 2˚ auditory cortex
is formed by the stria vascularis. It is high in K+. ∞ Sound travels from the cochlear to the superior olivary nucleus in the
Periplymph – found in scala vestibule and scala medulla where sound and pitch are compared. Then it travels in the
tympani. Produced from the CSF and blood plasma. It lateral leminiscus to the midbrain (I. colliculi) - auditory reflex?? Then
is high in Na+. to the thalmus (medial geniculate nucleus) and then to the auditory
Cochlear microphonics – is the ear is damaged it can cortex.
emit sound if the hair cells oscillate anyway.
The scala media has a Na+/K+ pump on it’s
membrane.
The spiral
ganglion
(cochlear
ganglion) is a
group of nerve

cells that sense

hearing and
send the
information to
the brain.
For more info on
cochlear With presbycusis higher frequencies are more affected so a patient needs
implants see a higher decibel to hear a given frequency. Noise related deafness is
info to right affected in this way (see below) because 4kHGz is the resonant greq
(normal freq of ear), so when this freq hits the ear it is amplified so it is
louder and more damaged over lifetime.
EAR (P) The chorda tympani is a nerve that originates from the taste buds and
Rinne’s and Webber’s test – differentiates between travels through the middle ear, passing inbetween the malleus and incus
sensorineural and conductive hearing loss. to join the facial nerve and send taste info to the brain.
Sound can reach the cochlear in two ways: via the bones of the The stapedius
skull, or through tympanic membrane and ossicles. contracts when there
Webber’s: place tuning fork on centre of head and ask if they is a loud noise to
hear it more clearly in either ear. Should hear it equally. prevent the stapes
from over-vibrating. Sensorineural
Rinne’s is to place tuning fork on mastoid process and outside Conductive
E.g. protects from
external meatus; latter should be louder. own voice. Doesn’t hearing loss hearing loss
If Webber’s is abnormal (can hear more on one side than protect against a
other), then it’s either a sensorineural (on other side), or gunshot because
conductive (on that side). that takes 200ms
If Rinne’s is –ve (can hear better through mastoid process) for the brain to
and it’s the opposite ear to Webber’s weird ear it’s recognise the sound
and contract the Aged-related
sensorineural. If Same ear as Webber’s it’s conductive.
muscle. It works (presbyacusis)
Sensorineural hearing loss can be caused by: inflammation,
oxycitic drugs (asprin, diuretics, aminoglycoside antibiotics),
best at high hearing loss
trauma, tumour or idiopathic. frequencies.
 CASE 6 REVISION – COGNITIVE IMPAIRMENT

MENTAL CAPACITY (L) MEMORY AND AGEING

It’s a public heath and a scientific problem.
A person lacks capacity in relation to a matter if at that time  Can study via longitudinal or cross-sectional studies
they cannot make a decision for themselves because of an  Flynn Effect has shown that as families shrink in size, and people
impairment or disturbance of the mind. increase in height and nutrition; memory increases.
Note also the Mental Health Act that is more to do with  Longitudinal and cross sectional studies show different results;
people who have mental disabilities (temporary or both show a decrease in episodic memory but longitudinal studies
permanent that might cause them harm to themselves underestimate age related changes and cross-sectional ^estimate
or others). AGEING
The mental capacity act is time and situation specific. Short term memory declines; especially if info has to be manipulated
Mental capacity act really only applies broadly to those Episodic memory declines
over the age of 16 Semantic memory improves
This act doesn’t mean that they cannot make a decision Long term also declines(?)
ever, or that they cannot make any decisions at that Implicit memory – can learn new skills but perception speeds decline
time. They might have a temporary impairment or might The central executive is less prevalent
be able to make basic decisions but not more complex Cannot inhibit irrelevant info as easily (linked to central exec)
ones. Theories/hypothesis
The patient needs a diagnosis as having impairment or General mental slowing (Salthouse) – cognitive effects of ageing caused
otherwise it is presumed that they have capacity. by slowing of perception speed
The patient needs to be able to weight and retain Common Cause (Baltes) – everything in the body is slowing; incl
information to be considered to have capacity. perception and therefore this effects memory
KEY PRINCIPLES It’s more likely that there are multiple reasons why memory declines;
1. A person is to be assumed to have capacity until proven normal ageing and disease processes.
otherwise Risk factors: smoking, poor diet, poor physical fitness, intelligence,
2. Do everything you can to help them understand the education and social status.
choice/options.
3. You cannot decide they don’t have capacity because the Early life cognitive ability is biggest protective factor – reverse causation
decision is ‘unwise’. is thinking somebody has dementia when they’re just thick.
4. When acting for somebody without capacity you must act With age the ventricles expand, the frontal lobe shrinks rapidly, temporal
within their best interests. & occipital slowly and hippocampus slowly then rapidly in Alzheimer’s.
5. You should act in a way that least restricts their lives and Summary: frontal lobe problems cause normal aging (decreased
rights processing speed and working memory). Medial temporal lobe problems
BRAUU cause pathological problems incl. declarative/explicit memory.
Alzheimer’s
NEUOPSYCHOLOGY AND AGING (L) A type of dementia that causes a decline in intellectual abilities
Memory is knowledge that is stored in the brain; encoded, affecting ability to socialise and operate. Risk factors include age,
consolidated and stored and can be retrieved. smoking, intellectual ability and genetics (APOE-ε4). To have
Alzheimer’s you must have deficit in memory and either
Memory is a collection of mental abilities, utilising different memory perception or language or executive functioning. Causes
systems. Remembering requires diff processes and diff systems. anterograde amnesia. Declarative memory declines; episodic
Memory is a process of encoding; retrieval and storage more than semantic. Working memory declines but not so much
Atkinson & Shiffrin (1968) Three stage modal model of memory; is as declarative. Implicit memory can improve. Starts off affecting
that sensory info is put into short term memory, and when medial temporal lobes and hippocampus, and then parietal also.
rehearsed and consolidated, and is then put into long-term Hippocampus atrophies causing episodic memory loss.
Stage 1 (Sensory memory) is either iconic (visual) or echoic
(auditory) and is visual and fast Anterograde amnesia – cannot remember/encode new
Sperling (1960) Iconic memory – showed that when remembering information
12 letters; once recalled one row of them, have forgotten all of the Retrograde amnesia – cannot remember things that happened
others. If there’s a delay in recalling = likely to be less accurate. in the past
Stage 2 (Short term memory) is the memory of information held in Amnesia can be caused by temporal lobe surgery (deliberate),
the mind. Miller (1956) said 7 is the number of items most people herpes simplex encephalitis, anoxia/hypoxia, Alzheimer’s and
can hold in their heads. Although ranges 5-7. This memory is of Korsakoff (from alcohol).
limited duration (20sec) and capacity. E.g. HM had medial temporal lobes (involved in storing new
Working memory is basically STM but reflects that it is for the memories, sensory input, comprehending language, emotion
temporary storage of info for reasoning, learning & comprehension. and meaning) removed incl. hippocampus and adjacent cortial
There are three components of working memory: phonological loop regions. He had no more seizures but anterograde amnesia.
(storage and rehearsal of visual info), visuospatial sketchpad His short term was intact but not long term. Impairment occurs
(holding of visual images), central executive (controls the whole when short term memory capacity is reached. However could
system). learn new skills.
Stage 3 (Long term memory) – unlimited capacity; consolidation of Hippocampal amnesia affects explicit/declarative memory
material to create an almost permanent memory trace in the brain (semantic and epidsodic) but not implicit.
Stage 4 (Retrieval) – remembering and searching for a memory Explicit memory occurs in the medial temporal lobe, however
trace. Explicit memory recall depends on working memory which is not all LTM can occur in medial temporal for below reason:
inhibited during recall. Remote memory is usually memory from childhood, or many
Explicit memory – aka declarative; conscious thought goes into years previously. Preserved in amnesia. Ribot’s law.
recall. Branches = episodic (personal experiences/events) or This is because recent memories are stored in hippocampus,
semantic (facts or general knowledge). but over years are transferred to neocortex.
Implicit memory – aka non-declarative; unconscious recall such as Explicit /declarative memory = medial temporal and hippocamp
procedural (walking/driving) and classically conditioned (phobias Working memory problems = frontal lobe damage. But memory
and attitudes) not affected; only how they use memory. Poor organising,
Amnesia – intellect and perception is preserved but memory is planning and manipulation of data etc.
disordered; causes severe forgetfulness. Implicit/non-declarative = amygdala, cerebellum and motor c.
 CASE 6 REVISION – COGNITIVE IMPAIRMENT

DEMENTIA MCI AND ALZHEIMER’S

Symptoms: memory loss, poor concentration, forgetting Mild cognitive impairment is the intermediate state where the patient
names, poor thinking/reasoning, forgetting things that have isn’t fully cognitively intact, nor are they demented.
heard or read, getting lost or confused, getting angry or  Not everybody who has MCI will get Alzheimer’s
anxious about forgetfulness and possible changes in  Declarative memory is typically worse in those patients with MCI
behaviour. that will go on to develop Alzheimer’s
Treatment: Rivastigmine (PSNS/cholinergic agent),  Hippocampal changes occur about 3 years prior to MCI and 6 years
gelantamine (competitive and reversible AChE inhibitor and prior to AD
agonist of nAChR) and donepezil (AChE inhibitor)
Alzheimer’s HEARING DAMAGE
Build up of beta-amyloid protein plaques (extracellular). Also
TAU protein (pathological) that forms neurofibrillary tangles;
this is intracellular. There is also profound neuronal loss. It is
the most common type of dementia. Apoliprotein E on
chromosome 19 has been implicated in late-onset
Alzheimer’s. Familial Alzheimer’s is when it occurs in 30s or
40s. It is caused by putation in PSEN1/2 gene on Ch14 or APP
gene on chromosome 21 (which is why people with Down’s
are at higher risk of dementia). Gradual deterioration with
impaired visuospacial skills as well as normal dementia symps
Dementia with Lewy Bodies Stapedius is supplied by
Symptoms of Parkinson’s and Alzheimer’s. Lewy bodies are facial nerve so Bell’s
deposits of protein in neurones. They decrease the levels of palsy (CN7 palsy) can ^
doamine and ACh in the neurones. If the Lewy bodies are sensitivity to noise. The
more at the base of the brain they give motor symptoms but stapedius is activated
elsewhere they are more cognitive problems. Sleep problems, when we talk so that low
behavioural changes and differing motor and cognitive freq sounds which are
problems throughout the day are big clues. People with DLB transmitted by soft
are likely to develop Parkinson’s and vice versa. tissue and bone are
Vascular dementia attenuated.
Sudden onset with stepped deterioration. This is thought to be We can hear up to about
due to the fact that vascular dementia is lots of little 200 decibels. Human
haemhorrages in the brain. Also called multi-infarct dementia freq range is 20Hz-
because it’s like a series of little strokes – and can give similar 20kHz.
symptoms. More behavioural and motor problems than with A rise of 3dB decrease
Alzheimer’s. Galantamine in particular is used in vascular safe time at that noise
dementia. level by half.
Fronto-temperal dementia Tinitus is associated with
Also called Pick’s disease. It;s not very common but the frontal hair cell death or when
lobes controlling behaviour, language and emotion and the there is a lesion on the
temporal lobes controlling understanding of words are auditory nerve (benign
affected. There is a loss of neurones and NTs in these regions; acoustic neuroma).
they shrink. More in younger people (<65) and can affect The sound arises in the brain not the ear.
behaviour, speaking and semantic memory. Pick bodies Can also be due to glue ear, drugs, glue ear, turbulent blood flow etc.
(protein) may build up in these lobes. Noise-induced hearing loss occurs at ~4kHz because this is the resonant
freq at which consonants are produced. It is close to the resonance freq of
INVESTIGATIONS external ear (so sound travels more easily).
Drugs that cause tinnitus/hearing problems: salicylites (asprin and
 Dopamine transporters differentiates LBD from Alzh acetaminophen), NSAIDs, loop diuretics, aminoglycoside antibiotics (end
 MRI allows you to measure volumes of areas of the brain in ‘-icin’), chinchoa alkaloids (quinidine) and antineoplastics (chemo
 A functional MRI can show blood flow through the brain drugs).
 A CT can show cerebral atrophy and ventricular enlarge The threshold between temp and permanent hearing damage is unknown.
 Would use imaging techniques to differentiate It is thought to be due to: metabolic overload and increased free radical
Alzheimer’s and vascular dementia. prod from mitochondria, ^intracellular Ca2+, poor blood supply, apoptosis
 MOCA – 26 or higher is normal. of hair cells (that don’t regen) and hair cells physically damaged (although
 Mini-mental is similar but quicker than a MOCA. 18-23 is this isn’t believed anymore).
MCI and under 18 is bad dementia.