Neurology Exam Flashcards
1
Q
+ Rombergs test
A
Unsteady both - = cerebellar disease
+Rombergs - steady with eyes open and unsteady with eyes closed
- posterior column lesion
- peripheral neuropathy (in particular with loss of
- vestibular dysfunction
2
Q
Additional findings in gait exam
A
Upper limbs:
Arm swing (absent in Parkinson’s disease).
Weakness and posture e.g. in spasticity shoulder adduction, elbow, wrist and finger flexion.
Ability to stand on toes (tests for S1) & heels (tests for L4,5).
Ability to turn around (often requires several small steps in patients with small step gait, may highlight gait difficulties).
Heel to toe test, often not possible.
3
Q
Causes of an asymmetric gait?
A
Unilateral spasticity eg. motor stroke (circumduction, ext of hip/kneee/ankle, leg swings out in lateral arc), UL arm adducted + internally rotated, elbow and wrist fleed
Unilateral cerebellar lesions (veering to a side)
Unilateral foot drop eg. common peroneal, L5, unilateral stroke
4
Q
Causes of foot drop
A
Common peroneal nerve palsy Sciatic Lumbosacral plexus lesion L4/5 root lesion Peripheral motor neuropathy Distal myopathy MND Precentral gyrus lesion
5
Q
Causes of bilateral symmetric spastic gait?
A
Differentials for spasticity (bilateral UMN lesion) - Bilateral stroke - Hereditary spastic paraplegia (HSP) - Spinal cord lesion - Cerebral palsy MS
6
Q
Bilateral foot drop?
A
Peripheral sensorimotor neuropathy (CIDP/Charcot)
Marie Tooth (CMT)
Bilateral strokes
MND
7
Q
Differentials for a parkinsonian like gait?
A
Parkinson’s- shuffling, stopped posture, loss of swing and tremor UL
Parkinson’s like syndromes - PSP, drug induced
8
Q
DDx wide based gait?
A
Cerebellar ataxia
Sensory ataxia
Vestibular ataxia
Frontal ataxic gait (unlikely in ex)
9
Q
Findings in an UMN lesion?
A
Absence of muscle atrophy
Absence of fasciculations
Increased tone/spasticity or clasp knife tone
+/- clonus
Weakness: weaker anti-gravity muscles (eg. hip flex < hip ext, hip ext < knee flex, doriflex < plantarflex)
Hyperreflexia
Plantar reflex up going
10
Q
Findings in a LMN lesion?
A
Muscle atrophy
Fasciculations
Decreased tone/flaccidity
Pattern of weakness - hip ext < hip flex, knee flex < ext, plantarflex < dorsiflex)
Hyporeflexia or areflexia
Plantar downgoing
11
Q
Proximal myopathy
A
Muscle atrophy in affected muscles No fasciculations Normal tone Pattern of weakness - proximal muscles Normal reflexes Plantar reflex down-going
12
Q
Sensorimotor peripheral neuropathy
A
Sensorimotor peripheral neuropathy there may be a variable mix of glove/stocking distribution sensory loss and motor weakness in a symmetric distribution
Absent ankle jerks
13
Q
Findings in cerebellar lesions?
A
Cerebellar ataxic gait
Abnormal heel to shin test
Abnormal foot tapping
14
Q
Sensory findings
A
Note that pinprick/temperature fibres are carried in the spinothalamic column.
Joint position/vibration fibres are carried in the posterior column.
Light touch is a good screen but is non-discriminatory.
15
Q
Reflexes in LL exam
Knee Jerk (L3,4) Ankle jerk (S1,2) Adductor reflex (L2,3)
A
Absent reflexes (despite reinforcement) is seen in peripheral neuropathies and chronic demyelinating polyneuropathy (CIDP).
Hyporeflexia is in keeping with lower motor nerve lesions.
Hyperreflexia is in keeping with upper motor nerve lesions.
Patients with myopathies may have reduced reflexes due to loss of muscle bulk.
16
Q
Power
A
5 - Normal power 4+ - Submaximal movement against resistance 4 - Moderate movement against resistance 4- Slight movement against resistance 3- Moves against gravity but not resistance 2 - Moves with gravity eliminated 1 - Flicker only 0 - No movement
17
Q
LL Movement
A
Hip Flexion - L1/2 Hip Extension - L5/S1 Hip Adduction - L2/3 Hip Abduction - L4/5 Knee flexion - S1 Knee extension - L3/4 Ankle dorsiflexion - L4/5 Ankle plantarflexion - S1/S2 Ankle eversion - L5/S1 Ankle inversion - L5 Big toe extension - L5
18
Q
UL Movement
A
Shoulder abduction - C5 Elbow flexion - C5/6 Elbow extension - C7 Finger extension - C7 Finger flexion - C8 Finger abduction - T1
19
Q
Assessment of Tone
A
Normal tone. Hypotonia, flaccidity. Hypertonia: Clasp knife spasticity (pyramidal). Lead pipe rigidity (extra-pyramidal). Cogwheel rigidity (extra-pyramidal) Froment's maneuver refers to accentuation of cogwheel rigidity with contralateral arm movements seen in Parkinson's disease
20
Q
UL Reflexes
A
Biceps C5
Triceps C7
Brachioradialis C6
Finger jerk C8
Absent reflexes (despite reinforcement) is seen in peripheral neuropathies and chronic demyelinating polyneuropathy (CIDP).
Hyporeflexia in keeping with lower motor nerve lesions.
Hyperreflexia is in keeping with upper motor nerve lesions.
Patients with myopathies may have reduced reflexes due to loss of muscle bulk.
21
Q
Sensation
A
See photos - learn dermatomes + nerve distributions
22
Q
Observation in sensory lesions
A
Note the presence of atrophy:
Lower motor neuron lesions.
Peripheral nerve, plexus or root lesions.
Myopathies.
Fasciculations:
Lower motor neuron lesions.
Shiny, hairless skin, ulcers - suggest peripheral neuropathy.
Pes cavus (high arch and claw toes) may be seen in:
Charcot Marie Tooth.
Friedreich’s ataxia.
23
Q
Fundoscopy Findings
A
Diabetic retinopathy
Non-proliferative:
Cotton-wool spots or soft exudates: are nerve fibre layer infarcts.
Hard exudates are caused by lipid accumulation in or under the retina secondary to vascular leakage.
Intra-retinal haemorrhages and microaneurysms may also be seen.
Proliferative:
Neovascularisation may progress to fibrosis and retinal detachment
Hypertensive retinopathy:
Mild: narrowing of retinal arterioles also referred to as copper/silver wiring. Arteriovenous nicking or “nipping”.
Moderate – Haemorrhages, either flame or dot-shaped, cotton-wool spots, hard exudates, and microaneurysms.
Severe – Some or all of the above, plus papilloedema.
24
Q
Findings in diabetic neuropathy
A
Sensory ataxia
Romberg’s test may be +ve
Progressive loss of distal sensation in a globe and stocking distribution and in severe cases - motor weakness may be present
Ankle jerks may be lost
25
Expected findings in CIDP
Classic form: Symmetric, sensori-motor neuropathy with predominant motor neuropathy that results in both proximal and distal muscle weakness
Less common variants - asymmetric and/or sensory-predominant forms
Reflexes are generally absent or reduced
Typical findings include an ataxia gait with a +ve Romberg, loss of sensation in a glove + stocking distribution, muscle atrophy + weakness + globally absent/reduce reflexes
26
LL findings in MS
UMN signs, hyper-reflexia, spasticity, up going plantar
Occasionally reflexes are lost due to interruption to afferent motor reflex arce fibres
Cerebellar and sensory finding (which may be patchy) may also be present
27
Findings in third nerve palsy (. This is the "down and out" eye syndrome. It is characterised by ptosis, a down-and-out pupil, mydriasis, absent light reflex with intact consensual constriction of the opposite eye, and failure of accommodation)
Ptosis, inferolateral displacement of the ipsilateral eye.
Reduced adduction, elevation and depression of the affected eye.
A dilated non-reactive pupil (to direct or contralateral light reflex & accommodation). In diabetic mononeuritis pupillary sparing is often seen.
28
Causes of third nerve palsy and 4th nerve palsy
Tumours can compress the nerve anywhere along its path.
Cavernous sinus lesions.
Trauma.
Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the midbrain.
Mononeuritis multiplex e.g. diabetes (often with pupillary sparing).
Intracranial aneurysms, in particular posterior communicating artery aneurysms.
In occulomotor palsy - no direct pupil response but there is an indirect pupil response
29
Findings in trochlear palsy + causes
Weakness of downward eye movement with consequent vertical diplopia that is worse in the adducted eye position, but improved diplopia with head tilted to contralateral side (look to the nose then down).
Weakness of intorsion, in particular with eye abducted.
30
6th nerve palsy - findings + causes
Medial deviation of ipsilateral eye.
Inability to look laterally (abduct).
Common causes of palsy:
Tumours can compress the sixth nerve anywhere along its path. Acoustic neuromas can affect the 6th nerve.
Elevated intracranial pressure, a false localising sign.
Trauma.
Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the pons.
Mononeuritis multiplex e.g. diabetes.
31
5th nerve palsy findings + causes
Sensory abnormality with peripheral nerve OR descending nucleus distribution (pain & temperature).
Motor abnormality: asymmetry of jaw on opening or weakness with mastication.
Loss of corneal reflex.
Common causes of palsy:
Tumours can compress the nerve anywhere along its path.
Trauma.
Cavernous sinus lesions can affect the two superior divisions of the trigeminal nerve.
Haemorrhagic or ischaemic stroke and demyelinating disorders that affect the nerve nucleus in the pons or along its descending nucleus.
32
Findings in a 7th nerve palsy
Lower motor neuron lesions:
Weakness of upper and lower facial muscles.
Upper motor neuron lesions:
Weakness of lower facial muscles with sparing of upper facial muscles.
Loss of corneal reflex.
Decreased tearing
Hyperacusis.
Loss of taste sensation on the anterior 2/3rds of the tongue.
33
7th nerve- UMN and LMN causes
Common causes of lower motor neuron palsy:
Bell's palsy, idiopathic facial nerve palsy or facial nerve palsy of suspected viral aetiology is the most common cause of peripheral, lower motor neuron facial nerve palsy.
Sarcoidosis.
Herpes zoster infection.
Guillain-Barré syndrome.
Otitis media.
Lesions affecting nucleus of facial nerve in ipsilateral pons, e.g. stroke, acoustic neuroma, demyelinating lesions.
Common causes of upper motor neuron palsy:
Lesion affecting the contralateral upper motor neuron fibres (above nucleus to cerebral motor cortex).
34
8th (acoustic) nerve palsy - findings + causes
```
Hearing loss.
Vestibular ataxia.
Common causes of palsy:
Acoustic neuroma.
Trauma or inflammatory conditions along it path.
```
35
9th (glossopharyngeal) nerve palsy - findings + causes
Loss of taste in the posterior 1/3rd of the tongue.
Loss of pain and touch sensations in soft palate, and pharyngeal walls.
CN IX and CN X travel together, and their clinical testing is not entirely separable.
36
Vagus nerve - findings in palsy
Uvula deviation towards normal palate, may result from ipsilateral lower motor lesion of the vagus nerve OR contralateral upper motor neuron vagus nerve.
Through the recurrent laryngeal nerve to the vocal cords, hoarseness may develop.
Dysphagia, dysphonia and decreased gag reflex.
Due to its parasympathetic input, cardiac and gastrointestinal abnormalities may be seen with vagal lesions
Common causes of palsy:
37
Causes of 10th (vagus) nerve palsy
Trauma.
Tumour along its path.
Stroke, demyelinating lesions and tumours affecting the nucleus in the medulla.
Upper motor lesions of the 10th nerve tract, often as a component of a pseudobulbar palsy.
Motor neuron disease.
38
Accessory nerve- palsy + causes
Paralysis of sternocleidomastoid and trapezius.
Common causes of palsy:
Trauma.
Tumour along its path.
Stroke, demyelinating lesions and tumours affecting the nucleus in the medulla
39
12th nerve palsy + causes
Protrusion of tongue away from side of lesion for an upper motor neuron process and toward the side of the lesion for a lower motor neuron process.
Common causes of palsy:
Trauma.
Tumour along its path.
Stroke (e.g. medial medullary syndrome), demyelinating lesions and tumours affecting the nucleus in the medulla.
Upper motor lesions of the 12th nerve tract, often as a component of a pseudobulbar palsy.
Motor neuron disease.
40
Where are the cranial nerves in close proximity?
Midbrain: Nuclei of cranial nerves 3 and 4.
Pons: Nuclei of cranial nerves 5, 6, 7 and 8.
Medulla:Nuclei of cranial nerves 5 (descending nucleus), 9, 10, 11, 12.
41
Nerves in close proximity at the cerebellopontine angle?
```
Trigeminal nerve. 5/6/7/8
Vestibulocochlear nerve.
Facial nerve.
Abducens nerve
In addition, the pons, medulla and cerebellum are all in close proximity.
```
42
Cavernous sinus nerves
Sympathetic nerves, cranial nerves 3, 4, 6 and 5 (ophthalmic & occasionally maxillary divisions).
43
Lateral medullary syndrome
nystagmus (to side of lesion)
ipsilateral fifth (pain and temp), 9th and 10th CN lesions
ipsilateral cerebellar signs
contralateral pain + temp loss over the trunk and limbs
44
Nerves at the jugular foramen
Lower Cranial Nerves: 9, 10, 11 and 12.
45
Horizontal gaze palsy
Horizontal gaze centres are located in both the frontal lobe and pons.
Pontine lesion causes an ipsilateral gaze palsy
46
Causes of horners syndrome
```
Carcinoma of lung apex
Neck
Carotid arterial lesion
Brain stem lesions - vascular, syringobulbia, tumour
Retro-orbital lesions
Syringomyelia (rare)
```
47
Complex opthalmoplegia
Myasthenia gravis.
Mitochondrial myopathies.
Graves eye disease.
48
MS Findings
Depending on area of brain involved, can be: ng on the area of the brain involved the gait may be normal, impacted by weakness, spastic, ataxic or demonstrate foot drop.
Eyes: Optic neuritis and reduced acuity.
Fundoscopy may show optic atrophy.
Visual fields may show a defect and/or central scotomas.
Pupillary reflex may reveal a slow Marcus Gunn pupil (swinging light).
```
Brainstem involvement:
Motor weakness.
Diplopia.
Lower cranial nerve involvement.
Internuclear ophthalmoplegia.
Gaze palsies.
```
Transverse Myelitis - UMN below sensory level
Cerebellar signs - ataxic gait, limb incoordination, staccato/scanning, nystagmus
Sensory changes - Various sensory signs may be present:
```
Hyperaesthesia or paraesthesia.
Sensory loss.
Patchy sensory loss.
Sensory level in transverse myelitis.
Bladder and bowel dysfunction may also be present.
```
49
Findings in transverse myelitis
Upper motor neuron findings below the transverse myelitis level.
Sensory level.
50
CMT - dominant, myelin sheeth --> PNS
| Type 1-7
Chronic, slowly progressive, hereditary sensorimotor peripheral neuropathy but patient usually remains ambulant.
Most commonly - peroneal + tibial muscle
Asympt to 2 years - clumbsy/falling/tripping - Proprioception + motor
Normal life span
Clinical:
- Stork legs
- Pes cavus + claw toes + hands
Sensory - paresthesia - reduced muscle mass
Decreased pain (spinothalamic)
Decreased proprioception/vibration
Worse with vincristine, some anaesthetics + pregnancy
Nerve conduction velocity decreased
Sural nerve biopsy - diagnostic
Genetic testing
Mx - supportive, orthotics (ankle stability), PT (decrease frequency of ankle fractures), ankle fusion
Avoid drugs - vincristine, phenytoin/carbamezepine/anaes
51
CMT -LL + UL
Lower limbs:
Pes cavus.
Gait, high stepping sensory ataxic gait.
Distal muscle weakness & atrophy (inverted champagne bottle legs).
Reduced sensation in a glove/stocking distribution & reduced/absent reflexes.
Management with ankle-foot orthoses.
UL:
Atrophy and weakness of the small muscles of the hand.
Reduced sensation in a glove/stocking distribution & reduced/absent reflexes.
52
Causes of INO
most common causes of INO are multiple sclerosis and brainstem infarction. Other causes include head trauma, brainstem and fourth ventricular tumors, Arnold-Chiari malformation, infection, hydrocephalus, and lupus erythematosus
53
Myasthenia Gravis
Myasthenia gravis is an autoimmune condition with of the postsynaptic neuromuscular junction. Approximately 90% of patients with generalised MG are +ve for AchR- Ab, MuSK-Ab cor LRP4 antibody.
MG often presents with fatigability and may affect muscles generally and variably involve the respiratory, bulbar and ocular muscles.
54
MG Features Eyes
Ptosis can be unilateral or bilateral and fluctuate from one eye to the next.
Horizontal or vertical diplopia may result from muscle weakness. This may mimic a cranial nerve palsy or not conform to a nerve or gaze palsy.
Pupils are spared.
55
MG Features - facial + bulbar
Neck/Limb/Respiratory
Facial muscles may be involved leading yo a mask-like facies.
May present with fatigue while chewing, dysphagia and dysarthria.
Neck flexors and extensors may be affected.
Proximal limb muscles tend to be more affected.
Upper limbs are often more affected than the lower limbs.
Respiratory muscles may be involved and lead to respiratory failure.
56
Investigations in MG
```
AcHR ab
Anti-MuSK ab
LRP4 antibody
EMG - detrimental response
Tensilon test
CT - thymoma
```
57
Findings in IBM
Variable degrees of limb weakness + atrophy
IBM:
Note in particular atrophy of quadriceps muscles and long finger flexors.
Atrophy parallels duration & severity of weakness.
Reflexes decreased due to loss of muscle bulk.
Facial muscles may be involved, but oculomotor muscles are spared.
Dysphagia is seen in 30 - 50% of affected patients and occasionally precedes the weakness.
Some patients develop early quadriceps weakness & knee extensors are disproportionately weak as compared to the hip flexors, foot extensors also involved.
Weakness of the wrist and finger flexors is often greater than extensor weakness.
Usually symmetrical, (asymmetrical in 10-15%, myalgia in 40%).
58
Causes of anosmia
```
URTI
Meningioma olfactory groove
Head trauma
Meningitis
Hydrocephalus
Congenital - kallmann's
```
59
Causes of absent light reflex but intact accommodation reflex
Midbrain lesion (eg. A-R pupil)
Ciliary ganglion lesion (Adie's pupil)
Parinaud's syndrome
Bilateraly afferent pupil defects
60
Causes of absent convergence but intact light reflex
Cortical lesion
| Midbrain lesion
61
Eye constriction
```
Horner's
Argyll Robertson pipil
Pontine lesion
Narcotics
Pilocarpine drops
Old age
```
62
Eye dilation causes
```
Midriatics, atropine, cocaine
3rd nerve lesion
Adie's pupil
Iridectomy, irits
Post-trauma, cerebral death
```
63
Adie's syndrome
| Causes and signs
Lesion in the efferent parasympathetic pathway
Signs
- dilated pupil
- decreased or absent reaction to light
- slow or incomplete reaction to accomodation with slow dilation afterwards
- decreased tendon reflexes
- young women
64
Argyll Robertson Pupil
- Causes
- Signs
Syphilis, DM, Alcohol (rare), other midbrain lesions
Signs - small/irregular/unequal pupil
No reaction to light
Prompt reaction to accomodation
Decreased reflexes if tabes associated
65
Causes of papilloedema
Space occupying lesion
Hydrocephalus - obsturctive (tumour)
communicating
increased formation (choroid plexus papilloma)
decreased absorption - tumour causing venous compression, SAD obstruction from meningitis
```
BIH (idiopathic, OCP, addisons, drugs, lateral sinus thrombosis, head trauma)
HTN (Grade IV)
Central retinal vein thrombosis
Cerebral venous sinus thrombosis
High CSF protein level (GBS)
```
66
Causes of optic atrophy
```
chronic papilloedema
optic nerve pressure
glaucoma
ischaemia
familial - retinitis pigmentosa, leber's disease, friedrich's ataxia
```
67
Causes of optic neuropathy
MS
Toxic (eg. ethambutol, chlroquine, alcohol, nicotine)
Metabolic - Vit B12 def
Ischaemia - DM, temporal arteritis, atheroma
Familial - lebers
Infective - infectious mononucleosis
68
Cataracts
```
old age
diabetes/steroids
hereditary
occular
irradiation
trauma
```
69
Causes of ptosis
With normal pupils
- senile
- myotonic dystrophy
- glaucoma
- irradiation
- trauma
With constricted pupils
- horner's
- tabes dorsalis
With dilated pupils
- third nerve lesion
70
Causes of nystagmus
Causes of jerky nystagmus
- vestibular (chronic - to side of lesion)
- cerebellar (unilateral - to side of lesion)
INO (nystagmus in the abducting eye, with failure of adduction on the affected dside)
result of a MLF lesion
Vertical
- brain stem lesion - upbeat nystagmust - floor of 4th ventricle, downbeat mystagmus - foramen magnum
- toxic - phenytoin, eTOH
Pendular
- retinal (decreased macular vision)
- congenital
71
supranuclear palsy
loss of vertical gaze, sometimes downward gaze
- both eyes
- pupils often unequal
- no diplopia
- reflex eye movements intake
72
Progressive supranuclear palsy
loss of vertical gaze first, then upgaze, finally horizontal
| can be assoc: Pseudobulbar palsy, long tract signs, extrapyramidal signs, neck rigidity
73
what is parinauds syndrome?
causes?
loss of vertical upgaze often assoc. with convergence-retraction nystagmus + pseudo A-R pupils
Causes
Central - pinealoma, MS, vascular
Peripheral- trauma, DM, other vascular, idiopathic, raised ICP
74
causes of sensorineural deafness
degneration (presbycusis)
trauma (eg. high noise exposure, fracture)
toxins (aspirin, alcohol, streptomycin)
infection (congenital rubella, syphilis)
tumour (acoustic neuroma)
brain stem
vascular disease of the internal auditory artery
75
causes of conductive deafness
wax
otitis media
otosclerosis
pagets
76
causes of multiple cranial nerve palsies
```
nasopharyngeal carcinoma
chronic meningitis
BGS
brain stem lesions
arnold-chiari malformation
trauma
lesion of base of scull
MM - rare
```
77
causes of peripheral neuropathy
diabetes 30%, hereditary 30%, idiopathic 30%, all others 10%
- drugs and toxins
- eTOH
- metabolic - diabetes, uraemia, hypothyroid, poryphria
- immune mediated - GBS
- tumour - lung ca
- Vit B12/B1 def, B6 excess
- idiopathic
- CTD/vasculitis - SLE, PAN
- Hereditary
78
causes of predominantly motor neuropathy
```
GBS + CIDP
Hereditary motor + sensory (CMT - disease)
acute intermittent porphyria
diabetes
lead poisoning
MMN
```
79
causes of predominantly sensory
```
carcinoma
paraproteinaemia
Vit B6 intox
Sjogrens
DM
Syphilis
Vit B12 def
idopathic
```
80
causes of a PAINFUL peripheral neuropathy
acute - DM, PAN or connective tissue (SLE, RA)
| chronic - compressive neuropathies, sarcoid, acromegaly, leprosy, lyme, carcinoma, idiopathic
81
causes of thickened nerves
hereditary motor + sensory neuropathy
acromegaly
CIDP
amyloidosis
82
causes of fasciculaiton
benign, MND, motor root compression, malignant neuropathy
83
causes of an extensor plantar response + absent ankle jerk
causes of subacute defined degen (B12 def)
conus medullaris lesion
combination of UMN with cauda equina or peripheral neuropathy
syphilis
Friedrich's ataxis
DM
adrenoleukodystraphy
84
causes of brown sequard
```
MS
Angioma
GLioma
Trauma
Myelitis
most radiation
```
85
approach to proximal muscle weakness?
myopathy
MG
neurogenic - MND, polyradiculopathy
86
pain and temp loss only
```
syringomeylia
brown sequard (contralteral leg)
anterior spinal artery thrombosis
lateral medullary syndrome
peripheral neuropathy
```
87
vibration and proprioception loss only
```
subacute combined
brown sequard (ipsilateral leg)
spinocerebellar degeneration (friedrichs)
MS
tabes dorsalis
sensory neuropathy + ganglioopathy
peripheral neuropathy
```
88
causes of cerebellar disease - unilateral
```
space occupying lesion
ischaemia
paraneoplastic
MS
trauma
```
89
causes of cerebellar disease - bilateral
```
drugs
friedreich's ataxis
hypothyroid
paraneoplastic
MS
TRauma
arnold-chiari
eTOH
space occupying lesion
```
90
cerebellar - midline
paraneplastic, midline tumour
91
rostral vermis lesion - LL only
eTOH (most common)
92
UMN + cerebellar sins combined
Adolescence - spinocerebellar degeneration
Young adults - MS, suphilis, spinocerebellar, arbnold-chiari
Later life - MS, syringomyelia, ifnfarction, lesion, degeneration
93
causes of pes cavus
freidrich's ataxia
HMSN
Neuropathies in childhood
idiopathic
94
causes of chorea
```
huntingtons (AD)
sydenhams (rheumatic)
senility
wilsons
drugs
vasculitis or CTD eg. SLE
```
95
causes of parkinsons
idopathics
drugs
postencephalitis
other -toxins, wilsons, steele richardson, shy-drager, syphilis, tumour
96
classification of rremor
parkinsonism - resting
action (resolves at rest) - thyrotoxicosis, anxiety, drugs, familial, idiopathic
intention tremor (cerebellar disease - increases approching target)
cerebellar outflow tract tremor (abduction/adduction movements of UL with F-E of wrists)
