Neuro Flashcards
1
Q
meningeal vessels
A
Vessels coming off the external carotid artery
- Are in the extradural space - between bones of the skull and the dura
2
Q
bridging veins?
A
cross the subdural space - between the dura and arachnoid
3
Q
circle of willis?
A
- lies in the subarachnoid space (between the arachnoid and
pia)
4
Q
white matter v grey matter
A
White matter contains myelinated axons
• Grey matter contains cell bodies and no myelin sheaths
5
Q
frontal lobe?
A
Voluntary movement on opposite side of body
- Frontal lobe of dominant hemisphere controls speech (Broca’s area) & writing
(if right handed, then left hemisphere is dominant etc.) - Intellectual functioning, thought processes, reasoning & memory
6
Q
pariental lobe?
A
- Receives and interprets sensations, including pain, touch, pressure, size and
shape and body-part awareness (proprioception)
7
Q
temporal lobe?
A
- Understanding the spoken word (Wernicke’s - understanding), sounds as well
as memory and emotion
8
Q
occipital lobe?
A
Understanding visual images and meaning of written words
9
Q
passage of CSF
A
CSF is produced by ependymal cells in
the choroid plexuses of the lateral
ventricles (mainly)
- From the lateral ventricles it travels to the
3rd ventricle via the interventricular
foramen and then from the 3rd ventricle it
travels to the 4th ventricle via the cerebral aqueduct (Aqueduct of Sylvius)
- From the 4th ventricle it communicates with the subarachnoid space via the
median foramen of Magendie and the two lateral foramen’s of Luschka
- CSF is then absorbed via arachnoid granulations (VILLI) e.g. in the superior
sagittal sinus
10
Q
hydrocephalus
A
Abnormal accumulation of CSF in ventricular system
• Often due to a blocked cerebral aqueduct
11
Q
sympathetic - CNS -
A
• Leaves the CNS from the thoracic & lumbar regions (T1 - L2) of the
spinal cord
• Most of the ganglia lie close to the spinal cord and form two chains
of ganglia - one on each side of the cord - known as the SYMPATHETIC
TRUNKS
• Uses acetyl-choline (ACh) at preganglionic synapse where there are
nicotinic receptors
• At effector cell synapse the
neurotransmitter noradrenaline is
used where there are adrenergic
receptors (of which there are 5
subtypes)
• Supplies visceral organs and
structures of superficial body regions
• Contains more ganglia than the the parasympathetic division
• Its effects are amplified by the adrenal glands (FORMED BY THE
SYMPATHETIC DIVISION) which in turn release adrenaline directly
into the blood resulting in a high blood pressure & heart rate
12
Q
parasympathetic CNS
A
• Leaves the CNS from the brainstem & sacral portion of the spinal cord
• Cranial outflow:
• Comes from brain
• Preganglionic fibres run via; oculomotor nerve CN3 - to pupil, facial
nerve CN7 - to salivary glands, glossopharyngeal nerve CN9 - for
swallowing reflex & via the vagus nerve CN10 - to thorax & abdomen
- remember by 1973
• Cell bodies are located in cranial nerve nuclei in the brainstem
• Innervates the organs of the head, neck, thorax & abdomen
• Sacral outflow: Supplies the remaining abdominal and pelvic organs
• Ganglia lie within/very close to the organs that the postganglionic
neurones innervate
• Uses acetyl-choline (ACh) at the preganglionic neurone synapse
where there are nicotinic receptors
• Uses acetyl-choline (ACh)
at the effector cell synapse
where there are muscarinic
receptors
13
Q
somatic nerves>?
A
sensory & motor:
- Bodily segments
- Conscious
14
Q
branchial
A
motor only:
- 5 branchial arches
15
Q
autonomic
A
sensory & motor:
- Parasympathetic & sympathetic
- No conscious awareness
16
Q
upper motor neurones v lower motor neurones
A
• Upper motor neurone:
- The descending pathways and neurones that originate in the motor cortex
- Control the activity of the lower motor neurones
• Lower motor neurone -
known as ALPAH MOTOR NEURONES:
- Alpha motor neurones that directly innervate skeletal muscle that have cell
bodies lying in the grey matter of the spinal cord and brainstem
17
Q
spasticity?
A
• Upper motor neurone:
- The descending pathways and neurones that originate in the motor cortex
- Control the activity of the lower motor neurones
• Lower motor neurone - known as ALPAH MOTOR NEURONES:
- Alpha motor neurones that directly innervate skeletal muscle that have cell
bodies lying in the grey matter of the spinal cord and brainstem
18
Q
rigidity?
A
- Increased muscle contraction is continuous and the resistance to passive
stretch is constant
19
Q
how many spinal nerves?
A
Has 31 pairs of spinal nerves (segments):
- Cervical - 8 nerves
- Thoracic - 12 nerves
- Lumbar - 5 nerves
- Sacral - 5 nerves
- Coccyx - 1 nerve
20
Q
conus?
A
Conus (end of spinal cord) finishes BEFORE L2
21
Q
spinal nerve exits from cords?
A
- Cervical segments: around 1 vertebra HIGHER than their corresponding
vertebra [EXCEPY C8 which exits below one vertebra] - Thoracic segments: around 1-2 vertebra BELOW their corresponding vertebra
- Lumbar segments: 3-4 vertebra BELOW their corresponding vertebra
- Sacral segments: around 5 vertebra BELOW
22
Q
sensory innervation of hand - nerves?
A
- Little finer (ulnar nerve) - C8
- Index finger (median nerve) - C7
- Thumb - C6 - The thumb is C6, always remember this!
23
Q
cervicle nipple medial arm umbilicus knee perianal areal anus DERMANTOME
A
- Clavicle - C4
- Nipples - T4
- Medial side of arm - T1
- Umbilicus - T10
- Knee - L4
- Perianal area - S4
- Anus - S5
24
Q
ascending tracts?
A
- dorsal/medial leminicus columns
- spinothalamic
- spino-cerebellar
25
dorsal leminscal columns?
```
Consist of the Fasciculus cuneatus
& Fasciculus gracilis
• Carry proprioception, vibration &
fine touch
• Fasciculus cuneatus - LATERAL
and carries information from the
UPPER body to the cuneate
tubercle in the medulla
```
• Fasciculus gracilis - MEDIAL and
carries information from the LOWER
body to the gracile tubercle in the
medulla
Ascends to the medulla and then DECUSSATES to become the medial
lemniscus then ascends to the thalamus then to the SOMATOSENSORY
CORTEX
• Thus decussates AFTER LEAVING SPINAL CORD
26
spinothalamic
```
• LATERAL: pain & temperature
• MEDIAL/ANTERIOR: crude touch
• Ascends on the same side for 1 to 2
segments then DECUSSATE (substansia gelatinosa) before
ascending to the thalamus (unlike other
sensory modalities that travel to the
cortex, PAIN reaches consciousness in
the THALAMUS)
• Thus decussates SOON UPON ENTRY
INTO SPINAL CORD
• The tract terminates at the thalamus
• PAIN REACHES CONSCIOUSNESS AT
THE THALAMUS - unique
```
27
spino-cerebellar tract?
Posterior spinocerebellar tract: carries information on proprioception to
the IPSILATERAL INFERIOR CEREBELLAR PEDUNCLE
• Anterior spinocerebellar tract: carries information on proprioception to
the CONTRALATERAL SUPERIOR CEREBELLAR PEDUNCLE
• Both carry the same information so difficult to clinically differentiate
28
descending tracts?
Originate from the cerebral cortex and brainstem (UPPER MOTOR
NEURONES)
Divided into pyramidal and extrapyramidal:
29
pyramidal tracts
- 2 neurone pathway originating in the cerebral cortex of cranial
nerve nucleus (for facial innervation)
- DECUSSATE in the medulla and descend CONTRALATERALLY
- Neurones innervating our axial muscles (muscles of the trunk and
head) mostly DO NOT DECUSSATE
- Synapses with the cell bodies of the ventral horn of the spinal grey
matter
- E.g. Corticospinal tract
30
extra-pyramidal tracts?
- Originate in the brainstem and carry motor fibres to the spinal cord
- Responsible for involuntary autonomic control of all musculature
- E.g. Rubrospinal tract, Tectospinal tract & Vestibulospinal tract
31
corticospinal tract?
• Transmits control of voluntary
muscles (motor)
• Lateral corticospinal tract
(75%): pyramidal (MEDULLARY)
DECUSSATION - limb muscles
- Originates from the
contralateral motor cortex
• Medial (25%): DECUSSATES as it leaves via the anterior white commissure (a bundle of nerve fibres that cross the mid-line of
the spinal cord) - axial muscles (head & trunk - muscles needed
to keep upright et.)
- Originates from the
contralateral motor cortex
• Upper motor neurones (UMN) originate in the motor cortex - a UMN
lesion can occur anywhere from the cortex all the way down to the ventral
horn
• Neurones (cell bodies) located in the ventral horns project to limb and
axial muscles - these are the lower motor neurones (LMN)
32
Vestibulospinal tract:
* Muscle tone, balance & posture (by innervating antigravity muscles)
* Originates from vestibular uncles (CN8)
* NON-DECUSSATING thus IPSILATERAL
33
Tectospinal tract:
* Head turning in response to visual stimuli
* Originates from the tectum; superior (visual) colliculus
* DECUSSATES at the midbrain thus is CONTRALATERAL
34
rubrospinal
* Facilitates flexors and inhibits extensors - fine hand movements
* Originates from the red nucleus
* DECUSSATES at the midbrain thus is CONTRALATERAL
35
brown squard syndrome?
* Hemi-section of the spinal cord
* Ipsilateral & contralateral are in relation TO THE LESION
```
• Ipsilateral weakness (i.e. less motor
etc.) below the lesion - due to damage
to the ipsilateral descending motor
corticospinal tract (decussated at the
medulla already)
• Ipsilateral loss of dorsal column
proprioception below lesion - sine the
ascending tracts are damaged before
they could decussate in the medulla
• Contralateral loss of spinothalamic
pain & temperature below the lesion
since spinothalamic fibres decussate
just after entering cord within the spinal cord
```
* ***** Overall:
- Ipsilateral loss of; proprioception, motor & fine touch
- Contralateral loss of; pain, temperature & crude touch
36
olfactory nerve?
sense of smell
| - sensory
37
optic nerve?
vision
- sensory
- test -> snellen test
38
oculomotor
- motor
- parasympathetic
- test pupillary constriction and accommodation
PALSY -> down and out eye
39
trochlear?
innervetes superior oblique
| - motor
40
trigeminal
- sensory and motor
| - function -> Chewing Face and mouth touch and pain
41
abducens
lateral rectus
| - motor
42
facia nerve
- sensory and motor
- parasympathetic
- Controls most facial expressions Secretion of ears and saliva
- anterior 2/3 of tongue
43
vestibulochlear
- sensory
| - hearing
44
glossopharyngeal?
- sensory and motor
- parasympathetic
- taste (posterior 1/3)
- Senses carotid blood pressure
- Muscle sense –proprioception, sensory awareness of the bod
45
vagus nerve?
- motor and sensory
- parasympathetic
- senses aortic blood pressure
- Slows heart rate - Stimulates digestive organ
46
accessory nerve?
- motor
| - controls trapezius and sternocleidomastoid
47
hypoglossal nerve
- motor
| - Controls tongue movements
48
parasympathetic cranial nervers
1973
10, 9, 7, 3
49
cranial nerve brainstem nuclei location
- 3,4 - Midbrain
- 5,6,7,8 - Pons
- 9,10,11,12 - Medulla
50
Brocas area?
Broca’s area is the language area of the DOMINANT (normally left if right handed)
FRONTAL LOBE
- damage causes expressive aphasia -> they will understand what you are saying but unable to express words into meaningful language
51
Wernickes area?
Wernicke’s area is the comprehension area in the DOMINANT (normally left if right
handed) TEMPORAL LOBE and is responsible for understanding speech:
- comprehension aphasia -> difficult understanding but fluent speech that is scrambled
52
external and internal carotid
- External carotid supplies everything in
head & neck EXCEPT the brain
• Internal carotid supplies the brain ONLY!
53
internal carotid braches
```
- Anterior cerebral artery (ACA):
• Supplies motor cortex and top
of brain
• If there is ischaemic stroke in ACA the lower
limbs will be effected e.g. legs
```
- Middle cerebral artery (MCA):
• Supplies the majority of the outer surface of
brain
• If there is ischaemic stroke in MCA then the
region affected will be from the chin to the
hip
- Posterior cerebral artery (PCA):
• Supplies peripheral vision - ischaemic stroke will result in peripheral
vision loss but not macular vision
- - The PICA supplies the medulla (CN 9,10,11,12) and an emboli can result in
lateral medullary syndrome: dsypgaia, slurred speech, facial pain
54
where does common carotid arteries bifurcate
- The common carotid arteries BIFURCATE into the internal (larger than the
external) & external carotid arteries at C4:
55
visual fields from nasal and temporal
Fibres from the nasal portion (closest to the nose) of the retina (carrying the
TEMPORAL VISUAL FIELDS) cross at the optic chiasm which is located JUST
ANTERIOR to the PITUITARY INFUNDIBULUM
Fibres from the temporal portion (furthest from the nose) of the retina (carrying the
NASAL VISUAL FIELDS) do the same as mentioned above ↑
56
where do optic tracts go after optic chasm
The optic tracts carry the fibres posterolaterally around the cerebral peduncles to
terminate at the geniculate bodies of the thalamus
After the lateral geniculate body, the optic radiations split into two
• The fibres carrying information from the inferior portions of the retina (and thus the
SUPERIOR VISUAL FIELDS) travel by looping laterally through the TEMPORAL
LOBE to the visual cortex - this is known as MEYER’S LOOP. **VLS**
• The fires carrying information from the superior portions of the retina (and thus the
INFERIOR VISUAL FIELDS) travel by looping superiorly through the PARIETAL
LOBE to the visual cortex - this is knows as BAUM’S LOOP **AIM**
57
damage to optic chasm causes?
= Loss of
vision of the temporal visual fields - this is
called hemianopia
58
damage to left optic tract
Damage to the left optic tract = Loss of
vision of the temporal field of the left eye & the
loss of the nasal field of the right eye - another
type of hemianopia
59
damage to left Meyers loop
Damage to the left Meyer’s loop carrying
information from the inferior retina and thus the
SUPERIOR VISUAL FIELD resulting in loss of
vision in the superior nasal field of the left eye
and the superior temporal field of the right eye
60
damage to left Baums loop?
carrying
information from the superior retina and thus the
INFERIOR VISUAL FIELD resulting in loss of
vision in the inferior temporal field of the right
eye and the inferior nasal field of the left eye
61
where does spinal cord finish?
SPINAL CORD FINISHED AT L1
epidural below L1
62
best place for lumber puncture?
L3/4 or L4/L5
63
complication with where C3 runs?
• CN3 runs over the petrous apex of the
temporal bone:
- If there is a fracture or inflammation then
CN3 can get pushed against the bone
resulting in a CN3 nerve palsy resulting in
a FIXED DILATED PUPIL
64
cerebellar symtoms?
- Ataxia - loss of full control of body movements - limb unsteadiness
- Nystagmus - rapid eye movements
- Deficit is ON SAME SIDE AS CEREBELLAR LESION (IPSILATERAL)
65
what passes through cavernous sinus?
```
Oculomotor nerve (3)
• Trochlear nerve (4)
• Opthalmic trigeminal (5.1)
• Maxillary trigeminal (5.2)
• Carotid (INTERNAL)
• Abducens (6) - only one going medially
• Trochlear nerve (4)
```
66
3 main investigations for head injury?
- GCS - Glasgow coma scale - measure of level of consciousness:
• Score adds to 14 and consists of 3 categories:
- Motor response - most important
- Verbal response
- Eye opening response
- Look at lateralising signs;
• To identify which hemisphere issue is with
• For example can check painful stimuli response:
- Pinch behind ear and will see what side has issue e.g. the R hand
may come up but the L will not
Look at pupils for signs of raised ICP:
• Fixed dilated pupils - CN3 palsy
• Papilloedema
- Monitor vital signs
67
clinical management of head injury?
- IV MANNITOL a diuretic to reduce oedema and thus ICP
| - Management of seizures e.g Diazepam for status epilepticus
68
TIA?
Definition:
- A brief episode of neurological dysfunction due to temporary focal cerebral
ischaemia without infarction
<24 HRS
69
TIA, epidemiology?
M>F
| blacks more at risk
70
aetiology of TIA?
- Small vessel occlusion
- Atherothromboembolism from the carotid is the CHIEF CAUSE
- Cardioembolism resulting in MICROEMBOLI
- Hyperviscosity
71
risk factor for TIA?
- Age - risk increases with age
- Hypertension
- Smoking
- Diabetes
- Heart disease - valvular, ischaemic or atrial fibrillation
72
pathophysiology of TIA?
- The commonest cause of a TIA is cerebral ischaemia resulting in a lack of O2
and nutrients to the brain resulting in cerebral dysfunction - however in a TIA
this period of ischaemia is short-lived, with symptoms usually only lasting a
maximum of 5-15 minutes after onset, and then resolves with before
irreversible cell death occurs
- Symptoms that gradually progress suggest a different pathology such as
demyelination, tumour or migraine
73
clinical presentation of TIA?
- SUDDEN loss of function, usually lasting for minutes only, with complete
recovery and no evidence of infarction on imaging
- Site of TIA is often suggested by symptoms
- - 90% of TIA’s affect the anterior circulation (carotid artery):
• Supplies the frontal and medial part of the cerebrum
• Occlusion may cause a weak, numb CONTRALATERAL leg +/- similar, if
milder, arm symptoms
• Amaurosis fugax:
- Sudden transient loss of vision in one eye
- 10% affect the posterior circulation (vertebrobasilar artery):
• Diplopia - double vision
• Vertigo - the feeling that your surroundings are moving
74
investigations of TIA?
```
- Bloods:
• FBC - look for polycythaemia
• ESR - will be raised in vasculitis
• Glucose - to see if hypoglycaemic
• Creatinine, electrolytes
• Cholesterol
```
- Carotid artery doppler ultrasound to look for stenosis/atheroma
- MR/CT angiography if stenosis to determine extent
75
treatment of TIA?
ABCD2 score risk of stroke after TIA
* Age > 60yrs = 1
* Blood pressure > 140/90mmHg = 1
* Clinical features:
* Unilateral weakness = 2
* Speech disturbance without weakness = 1
* Duration of symptoms:
* Symptoms lasting more than 1hr = 2
* Symptoms lasting 10-59mins = 1
* Diabetes = 1
meds
- - Antiplatelet drug:
• ASPIRIN IMMEDIATELY + DIPYRIDAMOLE (↑cAMP and ↓ thromboxane
A2) for two weeks then lower dose
• P2Y12 inhibitor longterm e.g. CLOPIDOGREL
- Statin longterm e.g. SIMVASTATIN
- Control cardiovascular risk factors:
• Antihypertensives such as ACE-inhibitor e.g. RAMIPRIL or angiotensin
receptor blocker e.g. CANDESARTAN
76
stroke?
Syndrome of RAPID onset of neurological deficit caused by focal, cerebral,
spinal or retinal INFARCTION
- Characterised by RAPIDLY DEVELOPING signs of focal or global disturbance
of cerebral functions, lasting for MORE THAN 24HRS or leading to death
77
stroke epidemiology?
M>F
increasing age
higher in Asian and black African
78
aetiology of stroke?
- Ischaemic/infarction account for 80% of strokes
| - Haemorrhagic account for 17% of strokes
79
pathophysiology go stroke?
- Ischaemic (70%):
• Arterial disease and atherosclerosis is the main pathological process
- Haemorrhagic (17%):
• Hypertension resulting in micro aneurysm rupture (Charcot-Bouchard
aneurysms)
80
clinica presentation of stroke?
- Anterior cerebral artery (ACA) territory:
• Leg weakness (more likely than arm weakness
since more of leg in ACA
- Middle cerebral artery (MCA) territory:
• CONTRALATERAL ARM & LEG WEAKNESS
- hemianopia
- Posterior cerebral artery (PCA) territory - visual issues:
• CONTRALATERAL HOMONYMOUS HEMIANOPIA
(loss of half the vision of the same side in both
eyes
81
investigations of stroke?
- Urgent CT head/MRI head BEFORE TREATMENT:
• Urgent if suspected cerebellar stroke, unusual presentation (i.e.
alternative diagnosis likely), high risk of haemorrhage (low GCS and
signs of raised ICP)
• To rule out haemorrhagic stroke before starting thrombolysis
- Pulse, BP & ECG:
• Look for AF
- Bloods:
• FBC: look for thrombocytopenia & polycthaemia
82
treatment for stroke?
• Treatment:
- Maximise reversible ischaemic tissue:
• Ensure hydration
• Keep O2 sats > 95%
ischemic
• Give tissue plasminogen activator e.g. IV ALTEPLASE
• Then start antiplatelet therapy e.g. CLOPIDOGREL 24hrs after
thrombolysis
haemorragic
• Antiplatelets contraindicated
• Any anticoagulants should be reversed for Warfarin reversal use
BERIPLEX and VITAMIN K
• Control hypertension
• Manual decompression of raised ICP, can also reduce ICP by giving
diuretic e.g. MANNITOL
83
subarachnoid haemorrhage
- Spontaneous bleeding into the subarachnoid space - between the arachnoid
layer of the meninges and the pia mater
- Can often be catastrophic
84
subarachnoid haemorrhage
- Spontaneous bleeding into the subarachnoid space - between the arachnoid
layer of the meninges and the pia mater
- Can often be catastrophic
85
epidemiology of subarachnoid haemorrhage?
- Typical age 35-65
| - most common = berry aneurysm
86
aetiology of subarachnoid haemorrhage?
- Rupture of saccular aneurysms (80%) e.g. berry aneurysms
- Atriovenous malformation (AVM) (10%)
- no cause found eg, tumours or bleeding disorder
87
risk factors for subarachnoid haemorrhage?
- hyper tension
- family history
- PCKD, eheler danlos
- smoking
88
pathophysiology of subarachnoid haemorrhage?
- Most common cause is ruptured aneurysm which leads to tissue ischaemia
(since less blood can reach tissue) as well as rapid raised ICP as the blood
(fast flowing since arterial), acts like a space-occupying lesion, puts
pressure on the brain, resulting in deficits if not resolved quickly
89
clinical presentation of subarachnoid haemorrhage?
- SUDDEN ONSET severe OCCIPITAL headache - ‘thunder clap’, like being
kicked in the head, SEVERE PAIN 12/10!!
- Vomiting, collapse, seizures and coma often follow
- papiloedema
signs
- Kernig’s sign (unable to extend patients leg at
the knee when the thigh is flexed)
- Brudzinski’s sign (when patients neck is flexed
by doctor, patient will flex their hips & knees)
90
investigations of subarachnoid haemorrhage?
- ABG
- - Head CT - GOLD STANDARD DIAGNOSTIC:
• Detects >90% of SAH within 1st 48hrs
• Seen as a ‘star shaped lesion’ due to blood filling in gyro patterns
around the brain and ventricles
- lumber puncture - • Xanthochromia ( due to breakdown products of Hb -> bilirubin)
91
treatment of subarachnoid haemorrhage?
- Maintain cerebral perfusion by keeping well hydrated (IV FLUIDS) and aim
for BP < 160mmHg
- Administer Ca2+ blocker to reduce vasospasm and consequent morbidity
from cerebral ischaemia e.g. IV/ORAL NIMODIPINE
- Endovascular coiling:
• Preferred to surgical clipping since has lower complication rate where
possible
• Promotes thrombosis and ablation of aneurysm
• FIRST LINE TREATMENT
92
subdural haemorrhage?
• Caused by the accumulation of blood in the subdural space - between the
arachnoid and dura mater following rupture of a BRIDGING VEIN between cortex
and venous sinus (vulnerable to deceleration injury)
93
epidemiology of subdural haemorrhage
- MOST COMMON where patient has a small brain e.g. alcoholics or dementia
etc. or babies that have suffered a trauma or elderly that have brain atrophy
that makes the bridging veins more vulnerable
94
pathophysiology of subdural haemorrhage?
- Trauma either due to deceleration due to violent injury or due to dural
metastases results in bleeding from bridging veins between the cortex and
venous sinuses
- Bridging veins bleed and form a haematoma (solid swelling of clotted blood)
between the dura and arachnoid - this reduces pressure and bleeding stops
- Days/weeks later the haematoma starts to autolyse due to the massive
increase in oncotic and osmotic pressure thus water is sucked into the
haematoma resulting in the haematoma enlarging
- This results in a gradual rise in intra-cranial pressure (ICP) over many weeks
- Shifting midline structures away from the side of the clot and if untreated
leads to eventual tectorial herniation and coning (brain herniates through
foramen magnum - causes significant damage)
95
clinical presentation of subdural haemorrhage?
- Interval between injury and symptoms can be days to weeks or months
- Fluctuating level of consciousness (35%) +/- insidious physical or
intellectual slowing
- Sleepiness
- Headache
- Personality change
- Signs of raised ICP e.g. headache, vomiting, nausea, seizure and raised BP
96
investigations of subdural haemorrhage?
- CT head:
• Diffuse spreading, hyperdense CRESCENT SHAPED
collection of blood over 1 hemisphere:
- SICKLE/CRESCENT SHAPE DIFFERENTIATES subdural blood
from extradural haemorrhage!!
97
treatment of subdural haemorrhage?
- Assess and manage ABCs, prioritise head CT
- Stabilise patient
- IV MANNITOL to reduce ICP
98
extradural haemorrhage?
• Collection of blood between the dura mater and the bone usually cause by head
injury
99
aetiology of extradural haemorrhage?
- MOST COMMONLY due to a traumatic head injury resulting in fracture of the
temporal or parietal bone causing laceration of the MIDDLE MENINGEAL
ARTERY, typically after trauma to the temple
100
epidemiology of extradural haemorrhage?
- Usually occurs in young adults (rare < 2 and > 60)
101
pathophysiology of extradural haemorrhage?
- Blood accumulates RAPIDLY over minutes-hours between the bone and
dura
102
clinical presentation of extradural haemorrhage?
• Head injury
• Brief post-traumatic loss of consciousness or initial drowsiness
- Severe headache, nausea and vomiting, confusion and seizures - due to
rising ICP +/- hemiparesis (weakness of half the side of the body) with brisk
reflexes (faster than usual)
103
investigations of extradural haemorrhage
CT • Shows hyperdense haematoma that is biconvex/lense
shaped/lemon shaped and adjacent to the skull:
- Blood forms a more rounded shape compared with the sickle-
shaped subdural haematomas as the tough dural attachments to
the skull keep it more localised
104
treatment of extradural haemorrhage?
- ABCDE emergency management - asses and stabilise patient
| - Give IV MANNITOL if increased ICP
105
epilepsy?
- The recurrent tendency to spontaneous, intermittent, abnormal electrical
activity in part of the brain, manifesting in seizures
chronic disorder >2 seizures
106
epidemiology of epilepsy?
- <20 or >60 yrs
107
aetiology of epilepsy?
- 2/3rds are idiopathic often familial
- Cortical scarring:
• Head injury years before onset
• Cerebrovascular disease e.g. cerebral infraction or haemorrhage
• CNS infection e.g. meningitis or encephalitis
- Space-occupying lesion e.g. tumour
- Stroke
- Tuberous sclerosis
- Alzheimer’s or dementia - epilepsy more common
- Alcohol withdrawal
108
pathophysiology of epilepsy?
• Prodrome:
- Lasting hours or days may rarely precede the seizure
- Not part of the seizure, results in change of mood or behaviour
• Aura:
- Part of seizure where the patient is aware and may precede its
other manifestations
• Post-ictally (after seizure):
- Headache, confusion, myalgia and a sore tongue
109
main two types of seizures?
• Primary generalised (40%):
- Simultaneous onset of electrical discharge
throughout whole cortex (involving both
hemispheres), with no localising features referable to
only one hemisphere
• Partial/focal seizures (57%):
- Focal onset, with features referable to a part of
one hemisphere e.g. temporal lobe
110
types of generalised seizures?
Generalised tonic-clonic seizure (aka grand-mal):
- Often no aura
- Loss of consciousness
- Tonic phase:
• Rigid, stiff limbs - person will fall to floor if standing
- Clonic phase:
• Generalised, bilateral, rhythmic muscles jerking lasting
seconds-minutes
Typical absence seizure (aka petit mal):
- Usually a disorder of childhood
- Child ceases activity, stares and pales for a few seconds only
Myoclonic seizure:
- Sudden isolated jerk of a limb, face or trunk
Tonic seizure
- Sudden sustained increased tone with a characteristic cry/grunt
- Intense stiffening of body (tonic)
Atonic (akinetic) seizure:
- Sudden loss of muscle tone and cessation of movement resulting
in a fall
111
types of partial seizures?
Simple partial seizure:
- Not affecting consciousness or memory
Complex partial seizure:
- Affecting awareness or memory before, during or immediately
after the seizure
- Most commonly arise from the temporal lobe (understanding
speech, memory & emotion)
112
Characteristics depending on which lobe is involved ?
Temporal lobe (memory, emotion & speech understanding):
- Aura (80%) - Deja-vu, auditory hallucinations, funny smells, fear
- Anxiety or out of body experience, automatisms
Frontal lobe (motor and thought processing):
- Motor features such as posturing or peddling movements of the
leg
```
Parietal lobe (interprets sensations):
- Sensory disturbances - tingling/numbness
```
```
Occipital lobe (vision):
- Visual phenomena e.g. spots, lines or flashes
```
113
investigations for epilepsy?
- Electroencephalogram (EEG):
• NOT DIAGNOSTIC
• Performed to support diagnosis of epilepsy when history suggests it
- MRI and CT head
114
treatment of epilepsy?
• Ensure patient harm themselves as little as possible - ABCDE
• Check glucose
• Prolonged seizure (longer than 3 minutes) or repeated seizures are
treated with RECTAL/IV DIAZEPAM or LORAZEPAM
generalised seizures
ORAL SODIUM VOLPORATE (not used in pregnant women), ORAL LAMOTRIGINE
partial seizures
CARBAMAZEPINE - 1st line
- surgery
- vagal nerve stimulation
115
dementia?
A syndrome caused by a number of brain disorders (e.g. Alzheimer’s) which
cause memory loss, difficulties with thinking, problem-solving or language
as well as difficulties with activities of daily living
116
epidemiology of dementia?
- Rare under 55 yrs
- Prevalence rises with age
- AD is more common in FEMALES than males
- Vascular and mixed dementias are more common in MALES than females
117
Alzheimer's disease?
• Most common cause
• Degeneration of the cerebral cortex, with cortical atrophy
• Accumulation of beta-amyloid peptide, a degradation product of
amyloid precursor protein, results in progressive neuronal damage,
neurofibrillary tangles, increases in the number of amyloid plaques and
the loss of ACh (neurotransmitter)
118
vascular dementia?
• Brain damage due to cerebrovascular disease; either major stroke,
multiple smaller unrecognised strokes (multi-infarct) or chronic
changes in smaller vessels
• Presents with signs of vascular pathology e.g. raised BP, past strokes
and focal CNS signs
119
Lewy body dementia?
• 3rd most common cause of dementia
• Deposition of abnormal protein within neurons in the brain stem and
neocortex
• Presents with fluctuating cognitive impairment, details visual
hallucinations
• ASSOCIATED WITH PARKINSONS!
120
frontal-temporal dementia?
• Specific degeneration/atrophy of the frontal and temporal lobes of the
brain
• Behavioural & personality change, early preservation of episodic
memory and spatial orientation, emotional unconcern, lowers
inhibitions
• Mixed dementia
• PARKINSON’S dementia
121
clinical presentation of dementia?
AD
- short term memory loss
- decline in language, agnosia and in motor skills
vascular
- history of TIA or stroke
- athropathy
Lewy body
- fluctuating cognition
- visual hallucination
122
investigations of dementia
- History - assess cognitive functions by asking various questions
- Mini Mental State Examination (MMSE) commonly used to screen for
cognitive function: <24
- blood tests
- brain CT
- PET scanning
123
treatment for dementia?
no specific therapy
prevention; healthy behaviours
support; socially and cognitive activities
medications; ORAL DONEPEZIL or ORAL RIVASTIGMINE
124
Parkinson's disease?
• Degenerative movement disorder caused by a REDUCTION IN DOPAMINE IN THE
SUBSTANTIA NIGRA
125
triad of Parkinson's?
- Rigidity
- Bradykinesia (slow to execute movement)
- Resting tremor
126
epidemiology of parkinsons?
- Increasing prevalence with age
- Peak age of onset is 55-65 yrs
- More common in MALES than females
127
aetiology of Parkinson's disease?
- Idiopathic
- Drug induced
- Combination of:
• Environmental factors - pesticides, methyl-phenyl tetrahydropyridine
(MPTP) - found in illegal opiates
• Parkinson genes - mutation in parkin gene and alpha-synuclein gene
• Oxidative stress and mitochondrial dysfunction
128
what is the basal ganglia made up of?
```
• Striatum (composed of the putamen & caudate
nucleus)
• Globus pallidus (external & internal)
• Substantia nigra
• Subthalamic nucleus
```
129
Parkinsons disease pathophysiology
- The substantia nigra produces DOPAMINE
- Parkinsons results from mitochondrial dysfunction and oxidative stress
- This results in the progressive degeneration of DOPAMINERGIC NEURONES
from the pars compacta of the substantia nigra in the midbrain that project to
the striatum (caudate and putamen) of the basal ganglia
- This results in reduced striatal dopamine levels due to the loss of
dopaminergic neurones
- Less dopamine means that the thalamus will be inhibited resulting in a
DECREASE IN MOVEMENT and thus the symptoms of Parkinson’s
130
clinical presentation of parkinsons disease?
- Onset of symptoms is gradual and commonly presents with impaired
dexterity or unilateral foot drop
- Onset is ASYMMETRICAL - ONE SIDE ALWAYS WORSE THAN THE OTHER
- it can first present as anosmia, depression and anxiety, aches, urinary urgency
- triad; tremor, rigidity and bradykinesia
131
investigations of parkinsons?
- Diagnosis is CLINICAL, based on history and examination
- Can confirm by response to LEVODOPA
- MRI head:
• Initially normal but will show atrophy
132
treatment of parkinsons?
- The GOLD STANDARD treatment is ORAL LEVODOPA given alongside a
decarboxylase inhibitor e.g. CO-CARELDOPA or CO-BENELDOPA:
• Levodopa (L-dopa) is a precursor to dopamine, but dopamine CANNOT
CORSS the blood brain barrier whereas L-dopa CAN
• The decarboxylase inhibitor prevents peripheral conversion of L-dopa
to dopamine and therefore reduces the peripheral side effects as well as
maximising dose that crosses blood brain barrier
s/e -> nausea, vomiting, arrhythmia
long term l-dopa use -> reduced efficacy, dyskinesia
- Dopamine agonists e.g. ORAL ROPINIROLE or ORAL PRAMIPREXOLE:
• Used to delay starting L-dopa in the early stages
- Monoamine Oxidase B (MAO-B) inhibitors e.g. ORAL SELEGILINE or ORAL
RASAGILINE:
• These inhibit MAO-B enzymes which breakdown dopamine, thus they
result in a reduction of dopamine breakdown so dopamine remains for
longer
- Catechol-O-methyl transferase (COMT) INHIBITORS e.g. ORAL
ENTACAPONE or ORAL TOLCAPONE:
• These inhibit COMT which breaks down dopamine
133
huntingtons?
• Huntington’s is a cause of chorea and is a neurodegenerative disorder
characterised by the LACK of the inhibitory neurotransmitter GABA
• Chorea:
• A continuous flow of jerky, semi-purposeful movements, flitting from one
part of the body to another
• They may interfere with voluntary movements but cease during sleep
134
epidemiology of Huntingtons?
- AUTOSOMAL DOMINANT condition with full penetrance - all gene carriers
WILL DEVELOP DISEASE
- Presents in middle age initially with a prodromal phase of mild symptoms e.g.
irritability, depression and incoordination then progressing to psychiatric
and cognitive symptoms
135
aetiology of Huntingtons disease?
- MUTATION on CHROMOSOME 4 resulting in the REPEATED EXPRESSION
OF CAG SEQUENCE
136
pathophysiology of Huntingtons?
- Repeated expression of CAG sequence leads to the translation of an
expanded polyglutamine repeat sequence in the huntingtin gene (expressed
throughout the body), the protein gene product the function of which is
unclear - the expansion is thought to be a toxic ‘gain-of-function mutation’
- The more CAG repeats present, the earlier symptom onset:
- Progressive cerebral atrophy with marked loss of neurones in the CAUDATE
NUCLEUS & PUTAMEN of the basal ganglia - there is specifically loss of the
corpus striatum GABA-NERGIC and CHOLINERGIC NEURONS
- This results in DECREASED ACh & GABA SYNTHESIS in the striatum
137
clinical presentation of Huntingtons disease?
- Often prodromal phase of mild psychotic and behavioural symptoms
- Then chorea develops:
• Relentlessly progressive, jerky, explosive, rigidity INVOLUNTARY
movements - CEASES when sleeping
- dysarthria, dysphagia and seizures
138
investigations of Huntingtons?
- Diagnosis is mainly clinical
- Genetic testing - shows many CAG repeats - OVER 35
- - CT/MRI:
• Shows CAUDATE NUCLEUS ATROPHY and INCREASED SIZE of the
frontal horns of the LATERAL VENTRICLES (signs of brain matter
destruction)
139
treatment of Huntingtons?
* BENZODIAZEPINES
* SULPIRIDE - neuroleptic - depresses nerve function
* TETRABENAZINE - dopamine depleting agent
140
headache classifications
- Primary:
• No underlying cause relevant to the headache
• Examples include; migraine (20% of population), cluster and tension
headache (affect 99% in lifetime)
- Secondary
• There is an underlying cause
• Examples include; meningitis, subarachnoid haemorrhage, giant cell
arteritis and medication overuse headache
- TGN
141
migrane?
- Recurrent throbbing headache often preceded by an aura and associated
with nausea, vomiting and visual changes
- A migraine aura may affect the patients eyesight with visual phenomena such
as fortification spectra (zig-zag lines), shimmering or scotomas (black holes
in visual field), but may also result in pins and needles (tingling), dysphasia
and rarely weakness of limbs and motor function
142
epidemiology of migraine?
- Most common cause of EPISODIC HEADACHE (recurrent)
- More common in FEMALES than males
- In 90% onset if before 40yrs
143
triggers for migraines
CHOCOLATE
- Chocolate
- Hangovers
- Orgasms
- Cheese
- Oral contraceptives
- Lie-ins
- Alcohol
- Tumult - loud noise
- Exercise
144
pathophysiology for migraines?
- Genetic and environmental factors play a role
- Genetic factors play a role in causing neuronal-hyper-excitability
- Changes in brainstem blood flow lead to an unstable trigeminal nerve
nucleus and nuclei in the basal thalamus
- Cortical spreading depression - self-propagating wave of neuronal and glial
depolarisation that spreads across the cerebral cortex is thought to cause
the aura of migraine and leads to the release of inflammatory mediators
which impact on the trigeminal nerve nucleus
```
- This results in release of vasoactive neuropeptides including calcitonin-gene-
related peptide (CGRP) and substance P; this then results in the process of
```
neurogenic inflammation - vasodilation and plasma protein extravasation -
leading to pain that propagates all over the cerebral cortex
145
clinical presentation of migraines
- could have prodrome
- migrane without aura, unilateral, pulsing, severe pain on head that is aggravated by physical activeity. There may be photophobia
- migraine with aura -> 2 attacks that have visual and somatosensory disturbances
146
investigations of migraine
- Mainly clinical diagnosis
- Always examine:
• Eyes - for papilloedema and other eye issues using fundoscopy
• BP
• Head & neck (scalp, neck muscles and temporal arteries)
- Exclude other causes:
• Lab tests - CRP & ESR
• (CT/MRI)
- lumbar puncture
147
treatments of migraine?
- Reduce triggers e.g. avoid dietary factors
- Acute:
• DO NOT OFFER ERGOTS e.g.ergotamine or OPIODS
• Triptans e.g. SUMATRIPTAN:
• NSAIDs e.g. KETOPROFEN, NAPROXEN or ASPIRIN - good since less
chance of developing medication overuse headache
- Avoid paracetamol or ibuprofen
prevention; • Beta blocker e.g. PROPRANOLOL (not for asthmatics)
• Tricyclic anti-depressant e.g. AMITRIPTYLINE , S/E; drowsiness, dry
mouth and reduced vision
• Anti-convulsant e.g. TOPIRAMATE, S/E; reduced memory
148
tension headache, epidemiology
- The COMMONEST PRIMARY HEADACHE
- Can be episodic (<15 days/month) or chronic (>15 days a month for at least
3 months)
- No organic cause
149
clinical presentation of tension headache
```
- Episodic (<15 days/month) or chronic (>15 days a month for at least 3
months)
- Usually has one of the following:
• Bilateral
• Pressing/tight non-pulsatile
• Mild/moderate intensity
• +/- scalp muscle tenderness
```
- Without vomiting or sensitivity to head movement, no aura
- Not aggravated by physical activity
150
treatment of tension headaches?
- Reassurance and lifestyle advice e.g. regular exercise, avoidance of
triggers
- Stress relief e.g massage or acupuncture
- Symptomatic treatment for episodes occurring >2 days a week:
• ASPIRIN
• PARCETAMOL
• NSAIDs e.g. IBUPROFEN
• NO OPIOIDS
151
cluster headaches?
Most disabling of the primary headache disorders
152
epidemiology of cluster headaches?
- More common in MALES than females
- Affects adults, typically between 20-40 yrs
- Commoner in smokers
153
pathophysiology of cluster headaches?
- Unknown
- May be due to superficial temporary artery smooth muscle hyper-reactivity
to serotonin (5-hydroxytryptamine - 5HT)
- There are hypothalamic grey matter abnormalities too
- Autosomal dominant gene has a role too
154
clinical presentation of cluster headaches?
- Abrupt onset
- Rapid onset of EXCRUCIATING pain AROUND ONE EYE, TEMPLE or
FOREHAND
- Ipsilateral cranial autonomic features:
• Eye may become watery and bloodshot with lid swelling, lacrimation,
• Facial flushing
- Pain is strictly unilateral and almost always affects the same side
- Rises to crescendo over minutes and lasts 15-160mins, once or twice a day -
usually at same time
- vomiting
155
investigations of cluster headaches?
Clinical diagnosis
156
treatment of cluster headaches?
- Acute attack:
• Analgesics are unhelpful
• 100% 15L O2 for 15mins via non-rebreathable mask (not if COPD)
• Triptan (selective serotonin (5HT) agonist) e.g. SC SUMATRIPTAN
prevention
• Calcium channel blocker e.g. VERAPAMIL is first line prophylaxis
• Avoid alcohol during cluster period
• Corticosteroids e.g. PREDNISOLONE may help during cluster
157
TGN?
• Trigeminal neuralgia is described as a chronic, debilitating condition resulting in
intense and extreme episodes of pain
3 parts to TG nerve (motor and sensory)
- CN5.1 - OPTHALMIC
- CN5.2 - MAXILLARY
- CN5.3 - MANDIBULAR
158
epidemiology of TGN?
- Peak incidence between 50-60yrs
- More common in FEMALES than males
- Prevalence increases with age
159
aetiology of TGN? - In most cases is due to compression of the trigeminal nerve by a loop of
vein or artery
- Can be due to local pathology such as aneurysms, meningeal inflammation,
tumours e.g. vestibular schwannoma - local pathology is more common in
YOUNGER PEOPLE as cause of compression
160
pathophysiology of TGN?
- Compression of the trigeminal nerve results in demyelination and excitation
of the nerve resulting in erratic pain signalling
161
clinical presentation of TGN?
- ALMOST ALWAYS UNILATERAL
| - At least 3 attacks of unilateral facial pain
162
investigations of TGN?
- In order to diagnose needs to be at least 3 attacks with unilateral facial pain
- Clinical diagnosis based on criteria above and based on history
- MRI to exclude secondary causes or other pathologies
163
treatment for TGN?
- Typical analgesics and opioids DO NOT WORK
- Anticonvulsant e.g. ORAL CARBAMAZEPINE suppresses attacks in most
patients
- Other, less effective options e.g. ORAL PHENYTOIN, GABAPENTIN and
LAMOTRIGINE
surgery;
• Microvascular decompression:
- Anomalous vessels are separated from the trigeminal root
• Gamma knife surgery:
- Directly at trigeminal nerve ganglion or nerve root
164
giant cell arthritis?
• Systemic immune-mediated vasculitic affecting medium to LARGE size arteries
of the aorta and its extra cranial branches
• ASSOCIATED with POLYMYALGIA RHEUMATICA (PMR) and can occur in 50% of
cases with GCA
165
epidemiology of giant cell arthritis?
- PRIMARILY in those OVER 50yrs
- Most common in caucasians
- More common in FEMALES than males
166
pathophysiology of giant cell arthritis?
- There is granulomatous arteritis of unknown aetiology affecting in particular
the extra-dural arteries and the large cerebral arteries specifically
- Arteries become inflamed, thickened and can obstruct blood flow
- Cerebral arteries affected in particular e.g. temporal artery
- Opthalmic artery can also be affected potentially resulting in permanent or
temporary vision loss
167
clinical presentation of giant cell arthritis?
- Severe headaches (temporal pulsating)
- Tenderness of scalp (combing hair can be painful) or temple
- Claudication of the jaw (pain in jaw) when eating
- SUDDEN PAINLESS VISION LOSS - EMERGENCY - Arteritic anterior
ischaemic optic neuropathy - optic disc is very pale/swollen
168
investigations of giant cell arthritis?
- Diagnostic criteria - 3 or more of:
• Over 50
• New headache
• Temporal artery tenderness or decreased pulsation
• ESR and CRP raised
• Abnormal artery biopsy - inflammatory infiltrates present
- Temporal artery biopsy:
• DEFINITIVE DIAGNOSTIC TEST
• Should be taken BEFORE or within 7 days of starting high dose
corticosteroids
169
treatment of giant cell arthritis?
- HIGH DOSE CORTICOSTEROIDS RAPIDLY e.g. ORAL PREDNISOLONE to
stop vision loss - gradual reduction of steroids over 12-18 months
- If visual symptoms persist then give IV METHYLPREDNISOLONE for 3 days
- Used long-term so give GI and bone protection (to prevent osteoporosis due
to steroid use) e.g. LANSOPRAZOLE and ALENDRONATE and Ca2+ and
vitamin D
170
paraplegia
| hemiplegia
* Paraplegia - paralysis of BOTH LEGS ALWAYS caused by spinal cord lesion
* Hemiplegia - paralysis of ONE SIDE of body caused by lesion of the brain
171
UMN signs?
signs are CONTRALATERAL to lesion
• Indicate that the lesion is above the anterior horn cell i.e. in the spinal
cord, brainstem and motor cortex
• Increased muscle tone - SPASTICITY:
• Weakness:
• Increased reflexes, they are brisk - HYPERREFLEXIA
172
LMN signs?
• Indicate that the lesion is either in the anterior horn cell or distal to the
anterior horn cell i.e. in anterior horn cell, plexus or peripheral nerve
• Decreased muscle tone
• WASTING (atrophy) +/- FASCICULATIONS (spontaneous involuntary
twitching)
• Reflexes are reduced or absent
173
- Spondylolisthesis:
• Slippage of one vertebra over the one below
• Nerve root comes out ABOVE the disc, therefore root affected will be the
one BELOW the disc herniation e.g. L4/L5 herniation leads to L5 nerve
root compression
174
- Myelopathy:
* Caused by spinal cord compression
* Upper motor neurone signs e.g. spasticity, weakness, hyperreflexia
* Spinal cord disease
175
- Radiculopathy:
```
• Caused by spinal root compression
• Lower motor neurone signs e.g. decreased muscle tone, wasting,
weakness and fasciculations
• Pain down dermatome supplied by root
• Weakness in myotome supplied by root
```
176
myelopathy - spinal cord?
• Compression of the spinal cord resulting in upper neurone signs and specific
symptoms dependent on where compression is
177
aetiology of myelopathy?
- Vertebral body neoplasms - MOST COMMON CAUSE OF ACUTE
COMPRESSION:
• Secondary malignancy commonly from lung, breast, prostate,
myeloma, lymphoma
178
pathology of disc herniation and prolapse
• Disc herniation:
- When centre of disc (nucleus pulposus) has
moved out through the annulus (outer part of
disc) resulting in pressure on nerve root and
pain
```
• Disc prolapse:
- When nucleus pulposus moves and
presses against the annulus but it doesn't
escape outside the annulus
- Can produce a bulge in the disc which,
sometimes, can result in pressure (less
pressure than herniation) on nerve root
resulting in pain
```
179
clinical presentation of myelopathy?
- There is progressive weakness of the legs with upper motor neurone signs
e. g. CONTRALATERAL spasticity and hyperreflexia
- Bladder (and anal) sphincter involvement is late and manifests as
hesitancy, frequency and later as painless retention
- There is SENSORY LOSS BELOW the level of the lesion:
180
investigation of myelopathy?
- MRI:
• GOLD STANDARD
• Identifies the cause and site of cord compression
181
treatment of myelopathy?
- If malignancy then give IV DEXAMETHASONE (reduces inflammation/
oedema around malignancy and improves outcome) and consider more
specific therapy e.g. radiotherapy or chemotherapy
- Epidural abscess must be surgically decompressed and antibiotics given
182
Cauda equina syndrome?
• The cauda equina is formed by the nerve roots caudal (distal) to
the level of the termination of the spinal cord at L1/L2
183
aetiology of cauda equine?
- Herniation of lumbar disc - MOST COMMONLY at L4/5 and L5/S1
- Tumours/Metastases - see above
- Trauma
- Infection
- Spondylolisthesis
- Post-op haematoma
184
pathology of cauda equine?
- Nerve root compression CAUDAL (distal) to the TERMINATION of the spinal
cord at L1/2
- Usually large central disc herniations at L4/5 or L5/S1 levels
- Generally S1-S5 nerve root compression - important in bladder function
185
clinical presentation of cauda equina?
- Bilateral sciatica
- Saddle anaesthesia
- Bladder/bowel dysfunction
- Erectile dysfunction
- Variable leg weakness that is FLACCID & AREFLEXIC (LMN
signs)
186
investigations of cauda equina?
- MRI to localise lesion
- Knee flexion - test L5-S1
- Ankle plantar flexion (downwards) - test S1-S2
- Straight leg raising - L5,S1, root problem - people with acute disc can barely
get leg OFF bed
- Femoral stretch test - L4 root problem
187
treatment of cauda equina?
- Refer to neurosurgeon ASAP to RELIEVE PRESSURE or risk irreversible
paralysis/sensory loss/incontinence!!!!:
* Microdiscectomy - removal of part of the disc - may tear dura!
* Epidural steroid injection - more effective for leg pain
* Surgical spine fixation - if vertebra slipped
* Spinal fusion - reduces pain from motion and nerve root inflammation
188
MS?
• Chronic autoimmune, T-cell mediated inflammatory disorder of the CNS in which
there are multiple plaques of demyelination within the brain and spinal cord,
occurring sporadically over years
Disease of the CNS with oligodendrocytes targeted, NOT SCHWANN CELLS of
the PNS - affects the WHITE MATTER of brain
189
epidemiology of MS
- 20-40 yrs
- F>M
- white population >
190
aetiology of MS?
- Not understood
- Combination of genetic and environmental factors:
• Exposure to Epstein-barr virus (EBV) in childhood may predispose to
the later development of MS in a genetically susceptible host
• Low levels of sunlight and vitamin D may be a risk factor:
- Early exposure to sunlight/vit D is important and vitamin D status
relates to prevention of MS and fewer symptoms and fewer new
lesions on MRI in established MS
191
pathophysiology of MS?
- Autoimmune mediated demyelination at multiple CNS
(OLIGODENDROCYTES TARGETED) sites resulting in discrete plaques of
demyelination - affects WHITE MATTER of brain
- Thought to be T-cell mediated - T cells activate B cells to produce auto-
antibodies against myelin
- Once T lymphocytes cross the blood-brain barrier they can cause a
CASCADE of destruction to the neuronal cells in the brain
- This results in demyelination and thus conduction disruption along axons
- PNS myelinated nerves are NOT AFFECTED since their myelin is Schwann cell
based and these Schwann cells are unaffected since their myelin has different
antigens to that of the CNS produced by oligodendrocytes
- Repeated demyelination leads to axonal loss and incomplete recovery between
attacks
- Poor demyelination healing results in relapsing and remitting symptoms
192
types of MS?
- Relapsing & remitting (80%):
• MOST COMMON PATTERN of MS
• Symptoms occur in attacks (relapses) with onset over days and typically
recovery, either partial or complete, over weeks
• Periods of good health or remission are followed by sudden symptoms
or relapses
- Secondary progressive MS:
• Follows on from relapsing & remitting MS
• Late stage of MS that consists of gradually worsening symptoms with
fewer remissions
- Primary progressive MS (10-15%):
• Gradually worsening disability WITHOUT relapses or remissions
• Typically presents later and is associated with fewer inflammatory
changes on MRI
193
clinical presentation of MS?
```
- Unilateral optic neuritis:
• Pain in one eye on eye movement
• Reduced central vision
- Numbness of tingling in the limbs
- Leg weakness
```
- Brainstem demyelination:
• Diplopia, vertigo, facial numbness/weakness, dysarthria or dysphagia
194
investigation of MS?
Diagnosis requires TWO or more attacks affecting DIFFERENT PARTS of
CNS; that is 2 CNS lesions disseminated in time and space i.e. cannot
diagnose MS after one potential relapse
- MRI scan brain & cord:
• DIAGNOSTIC - if history matches
• 95% have periventricular lesions
- Lumbar puncture:
• CSF examination shows oligoclonal IgG bands in over 90% cases - but
these are not specific to MS
195
treatment for mS?
- Encourage stress-free life as possible since a reduction in stress can reduce
number of new lesions
- If poor diet and sun exposure then give VITAMIN D
- Acute relapse:
• IV METHYLPREDNISOLONE for less than 3 days can help shorten acute
relapse - use steroid sparingly and aim to use less than twice a year
- Frequent relapse:
• SC INTERFERON 1B or 1A are anti-inflammatory cytokines and can
help reduce relapses by 30% in active relapse-remitting MS and can
reduce lesion accumulation
- Monoclonal antibodies:
• IV ALEMTUZUMAB which is a CD52 monoclonal antibody that
targets T cells
- Symptomatic treatment:
• Spasticity - ALL anti-spasticity can result in WEAKNESS!
- Physiotherapy
- BACLOFEN - GABA analogue that reduces Ca2+ influx,
surpasses release of excitatory neurotransmitters
196
MYASTHENIA GRAVIS (MG):
• Autoimmune disease against NICOTINIC ACETYLCHOLINE RECEPTORS (AChR)
in the neuromuscular junction
197
epidemiology of MG
- F>M
- peak age in women 30
- in men = 60
198
aetiology of MG?
- If under 50 yrs, then MG is commoner in women
and is associated with other autoimmune disease
e.g. pernicious anaemia, SLE and rheumatoid
arthritis and THYMIC HYPERPLASIA
- If over 50 yrs, then MG is commoner in men and is
associated with THYMIC ATROPHY or THYMIC
TUMOUR, rheumatoid arthritis and SLE
199
pathophysiology of MG?
- Autoimmune disease mediated by antibodies to nicotinic acetylcholine
receptor - anti-AChR antibodies, interfering with the neuromuscular
junction via depletion of working post-synaptic receptor sites
- This is achieved by immune complex deposition of anti-AChR IgG and
complement at the post-synaptic membranes, causing interference with and
destruction of receptors
- This blocks the excitatory effect of ACh on the nicotinic receptors (since
there are less receptors) resulting in muscle weakness
200
clinical presentation of MG?
- Increasing muscular fatigue
- Muscle groups affected in order:
• Extra-ocular
• Bulbar - swallowing & chewing
• Face
• Neck
• Trunk
201
lambert eaton myasthenia syndrome?
• Paraneoplastic condition, most often seen with small cell lung cancer
• Causes defective ACh release at the neuromuscular junction resulting in
proximal limb weakness with some absent reflexes
• Weakness tends to improve after exercise - UNLIKE in MG
202
investigations for MG?
- Serum anti-AChR:
• Raised in 90%
- Electromyography (EMG) & Nerve conduction study (NCS):
• EMG will detect Myaesthenia Gravis:
203
treatment for MG?
- Symptom control:
• Anti-cholinesterase so more ACh remains in neuromuscular junction
e.g. ORAL PYRIDOSTIGMINE
- Immunosuppression:
• Used to treat relapses or if there is no response to pyridostigmine, start
LOW STARTING DOSE e.g. ORAL PREDNISOLONE
- Thymectomy - removal of thymus if onset < 50yrs and disease poorly
controlled with anti-cholinesterase’s
204
organisation of movement
1. Idea of the movement - association areas of cortex
2. Activation of upper motor neurones in the pre central gyrus
3. Impulses travel to lower motor neurones and their motor units (a alpha
motor neurone and all the skeletal fibres it innervates) via the coricospical
tract
4. Modulating activity of the cerebellum and basal ganglia
5. Further modification of movement depending on sensory feedback
205
regulation of muscle tone?
- Stretch receptors in muscle (MUSCLE SPINDLES) innervated by GAMMA
MOTOR NEURONES
- Muscle stretched → afferent impulses FROM muscle spindles → reflex
partial contraction of muscle
- Disease states e.g. spasticity and rigidity ALTER MUSCLE TONE by altering
the sensitivity of this reflex
206
MND?
• Cluster of major degenerative diseases characterised by selective loss of
neurones in motor cortex, cranial nerve nuclei and anterior horn cells
• Sometimes referred to as Amyotrophic lateral sclerosis (ALS) in other countries
207
epidemiology of MND?
- M>F
- >60 yrs
- can be familial; Linked to a mutation in the free radical scavenging enzyme superoxide
dismutase (SOD-1)
208
pathophysiology of MND?
- Degenerative condition affecting motor neurones, namely anterior horn cells
- There is relentless and unexplained destruction of upper motor neurones
and anterior horn cells in the brain and spinal cord
- Causes BOTH UMN and LMN dysfunction
- Upper & lower motor neurones are affected but there is NO SENSORY LOSS
or SPHINCTER DISTURBANCE - this is what distinguishes MND from MS and
polyneuropathies
- MND NEVER affects EYE MOVEMENTS - distinguishing it from myasthenia
gravis
209
clinical presentation of MND?
1. Amyotrophic lateral sclerosis (ALP) - UMN + LMN:
• MOST COMMON
• Loss of motor neurones in motor cortex & anterior horn of the
cord
• Weakness + UMN signs e.g upping plantars + LMN wasting/
fasciculation’s - usually in one limb
2. Progressive muscular atrophy (PMA) - LMN ONLY:
• LOWER MOTOR NEURONE ONLY presentation with weakness,
muscle wasting and fasciculation’s usually starting in one limb and
gradually spreading to involve other adjacent spinal segments
3. Progressive bulbar pasty (PBP) - LMN ONLY:
• Lower cranial nerves (CN 9,10,11,12) and nuclei initially ONLY
affected
• Dysarthria, dysphagia, nasal regurgitation of fluids and choking
are the presenting symptoms
4. Primary lateral sclerosis (PLS) - UMN ONLY:
• LEAST COMMON
• Loss of Betz cells in motor cortex
• Mainly UMN signs + marked spastic leg weakness, with
progressive tetraparesis and pseudobulbar palsy
210
investigations of MND?
- Diagnosed based on clinical findings:
• Definite: LMN + UMN signs in 3 regions
• Probable: LMN + UMN signs in 2 regions
- EMG
- MRI
- lumber puncture
211
treatment of MND?
- Antiglutamatergic drugs:
• ORAL RILUZOLE - an Na+ channel-blocker that inhibits glutamate
release
- Drooling - due to bulbar palsy (wasting of muscles of mastication):
• ORAL PROPANTHELINE or ORAL AMITRIPTYLINE
- Spasms:
• ORAL BACLOFEN
212
GBS?
• An acute inflammatory demyelinating ascending polyneuropathy affecting the
PERIPHERAL NERVOUS SYSTEM (SCHWANN CELLS TARGETED) following an
upper respiratory tract infection of GI infection
213
epidemiology of GBS?
- M>F
| - 15-35 and 50-75
214
aetiology of GBS?
- Campylobacter jejuni
- Cytomegalovirus (CMV)
- Mycoplasma
- Zoster
- HIV
- Epstein-Barr virus (EBV)
215
pathophysiology of GBS?
- GBS is usually triggered by infection e.g. Campylobacter jejuni, EBV or
cytomegalovirus (CMV)
- It is thought that these infectious organisms share the same antigens as
those on the Schwann cells (PNS), such as ganglioside GM and GQ1b,
leading to autoantibody mediated nerve cell damage formation via
molecular mimicry
- Nerve cell damage consists of damage to the SCHWANN CELLS and thus
demyelination resulting in the reduction in peripheral nerve conduction
resulting in an acute polyneuropathy
216
clinical presentation of GBS?
- 1-3 weeks post infection a SYMMETRICAL ASCENDING MUSCLE
WEAKNESS starts - this may advance quickly, affecting all limbs at once and
can lead to paralysis
```
- The PROXIMAL MUSCLES are more affected e.g. trunk, respiratory and
cranial nerves (ESPECIALLY CN 7)
```
- Sensory signs include paraesthesias - but there are very few sensory signs
- Reflexes are lost early in the illness
217
investigations of GBS?
- Nerve conduction studies (NCS):
• DIAGNOSTIC if matches with clinical examination
- Lumbar puncture - done at L4:
• CSF has raised protein but normal white cell count
218
treatment for GBS?
- VENTILATE
- IV IMMUNOGLOBULIN for 5 days:
• Decreases the duration and severity of paralysis
- Low-molecular weight heparin e.g. SC ENOXAPARIN and compression
stockings to reduce risk of venous thrombosis
219
6 mechanisms that causes nerve malfunction
1. Demyelination:
- Schwann cell damage leads to myelin sheath disruption
2. Axonal degeneration:
- Axon damage causes the nerve fibre to die back from the periphery
3. Compression:
- Focal demyelination at the point of compression causes disruption of
conduction
4. Infarction:
- Micro-infarction of vasa nervorum occurs in diabetes and arteritis such
as polyarteritis nodosa and eosinophilic granulomatosis with polyangitis
5. Infiltration:
- Infiltration occurs by inflammatory cells in leprosy and granulomas such
as sarcoid and by neoplastic cells (cancer)
6. Wallerian degeneration:
- Process that results when a nerve fibre is cut or crash and the distal part of the axon that is separated from the neurone’s cell body
degenerates
220
mononeurtis multiplex
if 2 or more peripheral nerves are
affected, when causes tend to be systemic - WARDS PLC:
- Wegener’s granulomatosis
- Aids/Amyloid
- Rheumatoid arthritis
- Diabetes mellitus
- Sarcoidosis
- Polyarteritis nodosa
- Leprosy
- Carcinoma
221
carpal tunnel?
• The most common mononeuropathy and entrapment
neuropathy
• Results from pressure and compression on the median
nerve as it passes through the carpal tunnel in the wrist
MOST COMMON IN FEMALES
222
aetiology of carpel tunnel?
- Usually idiopathic
- Usually in those over 30yrs
- Associated with:
• Hypothyroidism
• Diabetes mellitus
• Pregnancy (third trimester)
• Amyloidosis including in dialysis patients
• Obesity
• Rheumatoid arthritis
• Acromegaly
223
carpel tunnel presentaiton?
- Symptoms are intermittent and onset is gradual
- Aching pain in the hand and arm (especially at NIGHT) - can
wake patient up
- Paraesthesiae (tingling or prickling) in thumb, index, middle &
1/2 ring fingers + palm (median nerve distribution)
224
investigation of carpel tunnel?
- Electromyography (EMG):
• See slowing of conduction
- Phalen’s test:
• Patient can only maximally flex wrist for 1 minute
- Tinel’s test:
• Tapping on the nerve at the wrist induces tingling - but non-specific
225
treatment for carpel tunnel
- Wrist splint at night
- Local steroid injection
- Decompression surgery (carpal tunnel ligament is cut to reduce pressure)
226
what does median nerve innervate
LOAF
- 2 Lumbricals
- Opponens pollicis
- Abductor pollicis brevis
- Flexor pollicis brevis
227
ulner nerve compression?
• Most often, compression occurs at the epicondylar groove or
at the point where the nerve passes between the 2 heads of
flexor carpi ulnaris (true cubital tunnel syndrome)
signs; - Weakness/wasting of:
• Medial (ulnar side) wrist flexors
• Interossei - cannot cross the fingers in the good
luck sign
• Medial 2 lumbricals - claw hand
- Wasting of the hypothenar eminence (base of little finger) thus weak little finger abduction
228
sciatic nerve roots?
L4-S3
from L4-S1 -> common peroneal nerve
from L4-S3 -> tibial nerve
229
CN3 palsy?
- Ptosis - dropping eyelids
- Fixed dilated pupil - loss of PARASYMPATHETIC outflow from EDINGER
WESTPHAL NUCLEUS which supply pupillary sphincter and ciliary bodies -
lens accomadation
- - Eye down and out
```
- Causes:
• Raised ICP
• Diabetes
• Hypertension
• Giant cell arteritis
```
230
CN 4 palsy?
(Trochlear) palsy:
- Innervate superior oblique muscle and results in a head tilt to correct the
extortion that results in diplopia on looking down e.g. walking downstairs
- Causes:
• Trauma to the orbit - rare
231
CN 6 palsy?
(Abducens) palsy:
- Innervate the lateral rectus muscle thus eyes will be adducted
- Causes:
• MS
• Wernicke’s encephalopathy
• Pontine stroke - presents with fixed small pupils +/- quadriparesis
232
CN5 palsy?
- Jaw deviates to side of lesion
- Loss of corneal reflex
- Causes; trigeminal neuralgia (pain but no sensory loss), herpes zoster,
nasopharyngeal cancer
233
CN 7 palsy?
```
(Facial) palsy:
- Facial droop and weakness
- Causes:
• Bells palsy is the most common lesion of the facial nerve - will see
dribbling out the side of mouth
• Fractures of the petrous bones
• Middle ear infections
• Inflammation of the parotid gland - which facial nerve passes through
```
234
CN 8 palsy?
• CN 8 (Vestibulocochlear) palsy:
- Hearing impairment
- Vertigo and lack of balance
- Causes:
• The vestibulocochlear nerve runs very close to the bone
• Is also very affected by surrounding tumours - if a tumour arises in the
internal acoustic meatus then this will press on the vestibulocochlear
& facial nerve
• Skull fracture
• Toxic drug effects
• Ear infections
235
CN9 and CN10 palsy?
- Gag reflex issues
- Swallowing issues
- Vocal issues
- Caused by a jugular foramen lesion
236
autonomic neuropathy?
• Sympathetic and parasympathetic neuropathies may be isolated or part of a
generalised sensorimotor peripheral neuropathy
237
clinical presentation of autonomic neuropathy?
- Sympathetic:
• Postural hypotension - faints on standing, eating or hot bath
• Ejaculatory failure - Shoot
• Reduced sweating
```
- Parasympathetic:
• Erectile dysfunction - Point
• Constipation
• Nocturnal diarrhoea
• Urine retention
```
238
primary brain tumours?
- Majority are gliomas (glial cell in origin):
• Astrocytoma (85-90%)
• Olidgodendroglioma (5%)
239
risk factors of primary brain tumours?
- Primary tumours are more common in affluent groups
- Ionising radiation
- Vinyl chloride
- Immunosuppression
- Family history - genetics
240
pathophysiology of primary brain tumours?
Given enough time, ALL GLIOMAS will progress to become Glioblastoma
Multiforme (GBM) - EXCEPT - pilocytic astrocytoma
241
symptoms of primary brain tumour?
- symptoms of raised ICP; progressive headache, papilooedema, drowsiness
- progressive neurological deficit
- epilepsy and seizures
- lethargy
242
investigations of primary brain tumour?
- MRI and CT
- Bloods
- biopsy
**lumber puncture is contraindicated when there is possibility of mass lesion since withdrawing CSF can cause herniation -:> brain compression
243
treatment of primary brain cancer?
- Surgery to remove mass - if possible
- Chemotherapy for glioma:
• Given at SAME TIME as surgery and then for 1st 6weeks post-op
• E.g. TEMOZOLOMIDE
- ORAL DEXAMETHOSONE
244
secondary brain tumours?
• 10 times MORE COMMON than PRIMARY BRAIN TUMOURS
most common is NSCL
245
treatment of secondary Brian tumours?
- Surgery - if age< 75yrs
- Radiotherapy
- Chemotherapy
- Palliative therapy
246
```
meningitis
encephalitis
encephalopathy
neuorpathy
polyradiculopathy
myelitis
```
• Meningitis:
- Inflammation of the meninges
- Can be bacterial/viral/fungal
• Encephalitis:
- Inflammation of the brain
- Usually viral
• Encephalopathy:
- Reduced level of consciousness/diffuse disease of brain substance
- Usually non-infective with multiple aetiologies
• Neuropathy:
- Damage to peripheral nerves
- Diptheria, Guillan-Barre syndrome, leprosy and rabies
• Polyradiculopathy:
- Inflammation of the nerve roots e.g. cauda equina
- HIV, CMV, syphilis
• Myelitis:
- Inflammation of the spinal cord
247
meningitis epidemiology?
- Occurs in people of all age groups but more common in infants, young
children and the elderly
248
aetiology of meningitis?
- Adults and children:
• Neisseria meningitides - gram-NEGATIVE DIPLOCOCCI - transmitted by
droplet spread
- Pregnancy women/older adults:
• Listeria monocytogenes - found in cheese, why pregnant women told to
AVOID
- Neonates:
• Escheria coli
• Group B Haemolytic streptococcus - Streptococcus Agalactiae
```
- Immunocompromised:
• Cytomegalovirus
• Cryptococcus neoformans (fungi)
• TB - Mycobacterium tuberculosis
• HIV
• Herpes simplex virus
```
249
clinical presentation of meningitis?
Triad - Headache + neck stiffness + fever
- In acute bacterial infection:
• Onset is typically sudden
• Papilloedema:• Neck stiffness, positive Kernig’s & Brudzinski’s
sign can appear within hours
• Meningococcal septicaemia is associated with a
NON-BLANCHING PETECHIAL (test using glass
test) + PURPURIC SKIN RASH
VIRAL
• Benign, self-limiting condition lasting 4-10 days
• Headache may follow for some months
250
investigations for meningitis?
- Blood cultures BEFORE LUMBAR PUNCTURE
- Blood tests; FBC, U&E, CRP, serum glucose
- Lumbar puncture at L4 - if unable to perform within 30 mins give empirical
antibiotics!:
• Send for microscopy and sensitivity
• Can give headache, paresthesia, CSF leak and damage to spinal cord
RESULTS
- bacteria -> raised protein and low glucose
- viral -> normal protein and glucose
- CT head (can do before lumber puncture if >60 yrs and have seizures)
251
treatment for meningitis?
- IF YOU SUSPECT BACTERIAL MENINGITIS - START ANTIBIOTICS BEFORE
TESTS COME BACK!!
- Bacterial meningitis:
• IV CEFOTAXIME or IV CEFTRIAXONE - 3rd generation Cephalosporin
• Consider steroids e.g. ORAL DEXAMETHASONE to reduce cerebral
oedema
252
encephalitis epidemiology ?
Infection and inflammation of the brain parenchyma
- mainly viral
- in children and elderly
253
encephalitis epidemiology?
```
- Mainly viral:
• Herpes simplex virus 1 & 2
• Varicella zoster, Epstein Barr, Cytomegalovirus, HIV, mumps, measles
- Non-viral:
• Bacterial meningitis
• TB
• Malaria
```
254
clinical presentation of encephalitis?
- WHOLE BRAIN AFFECTED - problems with consciousness (global defect in
higher functioning as well as drowsiness etc.) compared to meningitis
- Insidious onset (days) or can be abrupt
- Triad: Fever + Headache + Altered mental status
- seizures
255
investigations of encephalitis?
- MRI:
• Shows areas of inflammation and swelling, generally in the temporal
lobes in HSV encephalitis
- Electroencephalography (EEG):
• Shows periodic sharp and slow wave complexes
- Lumbar puncture:
• CSF shows elevated lymphocyte count
256
treatment for encephalitis?
If viral e.g. herpes simplex or varicella zoster then IMMEDIATE TREATMENT
with anti-viral e.g. IV ACICLOVIR - even BEFORE the investigation results
are available
257
herpes zoster - shingles?
• Primary infection with VZV causes chickenpox, following which the virus remains
latent in sensory ganglia
• Development of shingles may indicate a decline in cell-mediated immunity such
as that due to age or malignancy
258
pathophysiology of shingles?
- Viral infection affecting peripheral nerves
- When latent virus is reactivated in the dorsal root ganglia it travels down the
affected nerve via the sensory root in DERMATOMAL DISTRIBUTION over a
period of 3-4 days
- Resulting in perineural and intramural inflammation
259
clinical presentation of shingle?
- Pain and paraesthesia in dermatomal distribution priced rash for days
- Malaise, myalgia, headache and fever can be present
- Can be over a week before eruption appears
- Rash - consists of papules and vesicles RESTRICTED to SAME
DERMATOME:
260
investigations of shingles?
- Clinical diagnosis
| - Eruption of rash is virtually DIAGNOSTIC
261
treatment of shingles?
- Oral antiviral therapy begun WITHIN 72HRS OF RASH ONSET:
| • ORAL ACICLOVIR X5 DAILY
262
complications of shingles?
• Opthalmic branch of trigeminal nerve - if damaged will affect sight!!
• Post herpetic neuralgia (PHN):
- Pain lasting for more than 4 months AFTER developing shingles
263
cerebellar - purkinje?
- The most important layer is the PURKINJE LAYER as this is the only output
of the cerebellum
- Purkinje cells have a tendency to discharge at very high frequency - when
holding posture, the purkinje cell layer is constantly firing
- Purkinje cell layer degeneration results in dysfunction & ATAXIA
264
symptoms of cerebellar dysfunction?
```
DANISH
Dysdiadochokinesia.
Ataxia (gait and posture)
Nystagmus.
Intention tremor.
Slurred, staccato speech.
Hypotonia/heel-shin test.
```
