Neuro Paces Flashcards

1
Q

How to test upper limb myotomes and peripheral nerve

A

C5- shoulder abduction
C6- elbow flexion and wrist extension
C7- elbow extension
C8- thumb extension
T1- finger abduction

Median - flexion and pronation
Ulnar- flexion of ring and little finger DIP, intrinsic muscles of the hand
Radial- extension

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2
Q

How to differentiate ulnar nerve palsy from C8/T1 pathology

A

Abductor pollicis brevis would be weak in a C8-T1 lesion, it is supplied by the median nerve
Normal sensation in T1 if ulnar lesion

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3
Q

What are the signs of an ulnar nerve palsy?

A
  1. Relevant scar
  2. ‘Ulnar claw’ Extension at 4th and 5th metacarpal phalangeal joint and flexion at distal joint
  3. Wasting of small muscles of the hand
  4. Weak abduction of fingers
  5. Normal strength in abductor pollicis brevis
  6. Altered sensation in ulnar distribution
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4
Q

Types of diabetic neuropathy

A
  1. Distal symmetric polyneuropathy - progressive distal sensory loss in a glove and stocking distribution results in axonal loss in nerve conduction studies, motor involvement in severe cases
  2. Autonomic neuropathy- postural hypotension, gastroparesis, gustatory sweating, resting tachycardia
  3. Diabetic amyotrophy- microvasculitis presents with asymmetric pain then weakness in the proximal leg along with weight loss
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5
Q

Causes of peripheral neuropathy

A

1) Metabolic
- Diabetes (chronic, sensory predominant, length dependent)
- B12, B1, B6 deficiency
- Uraemia
- Hypothyroidism
2) Infective
- HIV (distal sensory, often painful)
- Lyme disease
3) Immune
- CIDP (relapsing course, often not length dependent)
- Paraprotrinaemic (myeloma or MGUS)
- Connective tissue disease (RA, sjogren, SLE, sarcoidosis)
- paraneoplastic (most commonly lung ca
- GBS
4) Genetic
- Charcot Marie Tooth
- Acute intermittent porphyria
5) Toxic
- isoniazid
- pyridoxine
- lead
- chemotherapy

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6
Q

Investigating diabetic neuropathy

A

Nerve conduction studies show a sensory axonal loss with reduced or absent sensory nerve action potentials in a length- dependent manner with the legs being most affected

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7
Q

Management of diabetic neuropathy

A

Optimise diabetes control
Foot care
Pain management
Postural hypotension managed with fludrocortisone
GI symptoms with prokinetics and antiemetics

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8
Q

Clinic signs of hereditary sensory motor neuropathy (Charcot Marie Tooth)

A

Wasting of distal lower limb muscles with preservation of the thigh muscle bulk
Pes cavus
Stocking distribution sensory loss
High steppage gait due to foot drop and stamping due to loss of proprioception
Wasting of hand muscles
Palpable lateral popliteal nerve

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9
Q

What causes hereditary sensory motor neuropathy

A

Most common types are I (demyelinating) and II (axonal) therefore nerve conduction studies are useful

Autosomal dominant inheritance (test for PMP22 mutations in HSMN I)

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10
Q

Tests for HSMN

A

Nerve conduction studies
Genetic testing

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11
Q

Management of HSMN

A

Physiotherapist/ occupational therapist
Orthotics
Genetic counselling

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12
Q

Causes of predominantly sensory peripheral neuropathy

A

DM
Alcohol
Drugs eg. Isoniazid and vincristine
Vitamin deficiencies - b12 and b1

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13
Q

Causes of predominantly motor peripheral neuropathy

A

Guillain barre and botulism present acutely
Lead toxicity
Porphyria
HSMN

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14
Q

Causes of mononeuritis multiplex

A

DM
Connective tissue disease eg. SLE and RA
Vasculitis
HIV
Malignancy

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15
Q

What causes a central scotoma?

A

Optic nerve disease eg. Optic neuritis
Affects ipsilateral side

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16
Q

What causes a bitemporal haemianopia?

A

Chiasmal lesion
Upper fields worse affected in pituitary tumours
Lower fields worse affected in craniopharynhiomas

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17
Q

What causes a homonomous superior quadrantanopia?

A

Temporal lobe lesion

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18
Q

What causes a homonymous inferior quadrantanopia?

A

Parietal lobe lesion

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19
Q

What causes a homonymous hemianopia?

A

Post chiasmal lesion, the more congruous the more posterior the lesion is
A posterior cerebral stroke can cause macular sparing due to dual blood supply

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20
Q

What is the Pathophysiology of MS?

A

BBB is more permeable to immune cellls. T cells enter the CNS. T cells attack the myelin sheath leading to inflammation.

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21
Q

How does MS present?

A

Sensory- Parasthesia, hypoaesthesia, pain, MS hugs
Optic neuritis- diminished visual acuity, decreased colour perception, periorbital pain preceding vision loss
Weakness- exercised induced weakness is characteristic, UMN signs
Spasticity
Bladder dysfunction
Constipation
Sexual dysfunction
Uthoff’s phenomenon- symptoms worse after hot bath
Lhermitte’s sign- lightening pains down the spine on neck flexion due to cervical cord plaques

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22
Q

Disease course of MS

A

Relapsing remitting
Secondary progressive
Primary progressive

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23
Q

Differentials for MS

A

Inflammatory conditions- neuromyelitis optica, shortens, ADEM, CNS lupus/vasculitis
Infection - syphilis, Lyme disease, HIV
Metabolic- B12 deficiency, mitochondrial disease

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24
Q

Diagnosis and investigation of MS

A

Need to prove dissemination of disease activity in time and space.
1. Clinical history
2. MRI
3. Unpaired oligoclonal bands in the CSF (not specific for MS, occur in 85% of cases)

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25
Management of MS
Multidisciplinary approach DMARDs: - interferon B and glariramer reduce relapse rate but don’t affect prognosis, they are 1st line for mild disease - mabs offer greater benefit, used if 2 disabling relapses in 1 year Stem cell transplantation
26
Management of acute MS flare
Rule out psueudo relapse (ie. Worsening of existing symptoms by underlying stressor eg. Infection Methyl pred
27
Management of MS complications
Baclofen for spasticity Anti- depressants Neuropathic analgesics Antichoniergics/self catherisation for bladder symptoms
28
How is MS affected by pregnancy?
Reduced relapse rate in pregnancy Increased risk of relapse in postpartum
29
What causes MS?
Both genetic (HLA-DR2 and interleukin 2&7 receptors) + environmental factors (EBV)
30
Clinical signs of cerebellar syndrome
Dysdiadochokinesis Ataxia Nystagmus Intention tremor Scanning dysarthria Hypotonia/ hyporeflexia
31
How does the direction of nystagmus help determine side on the lesion?
The fast phase of the nystagmus is towards the side of the lesion and is maximal on looking towards the lesion
32
Causes of cerebellar syndrome
Stroke Paraneoplastic Alcoholic cerebellar degeneration Multiple sclerosis SOL in the posterior fossa Fredrich’s ataxia and ataxia telangiectasia Phenytoin toxicity Hypothyroidism
33
Clinical signs pointing to different causes of cerebellar syndrome
Internuclear ophthalmoplegia, spasticity, younger female = MS Optic atrophy = MS or Fredrichs ataxia Clubbing/ cigarette fingers, radiotherapy burn = bronchial carcinoma Liver disease = alcohol excess Neuropathy = alcohol or fredrichs ataxia Gingival hypertrophy = phenytoin
34
What happens in internuclear ophthalmoplegia?
The side of the brain affected is the same side as the eye that cannot adduct. Eg. A left sided lesion will result in the left eye not addicting when looking right and the right eye will have nystagmus. Caused by a lesion affecting the medial longitudinal fasciculus (a heavily myelinated tract).
35
How can you differentiate sensory ataxia from cerebella ataxia
Sensory ataxia - impaired sensation particularly vibration and joint position, pseudoathetosis, able to finger nose test with eyes open but not with eyes closed Cerebella ataxia - other cerebellar signs
36
How does ALS present?
UMN and LMN signs Upper limb weakness> lower limb weakness Fasciculations Asymmetrical Slurred speech Dysphagia/dysarthria
37
How does progressive bulbar palsy present?
Facial muscle weakness Dysphagia Dysarthria Emotional lability Upper and lower weakness
38
How does progressive muscular atrophy present
LMN Muscle atrophy Fasciculations Muscle weakness Best prognosis
39
How does primary lateral sclerosis present?
Spastic weakness of the limbs Spastic dysarthria Dysphagia Aggressive course
40
How is a case of suspected MND investigated?
Blood tests inc. vitamin levels, CK assay and anti-GM1 antibodies EMG showing Fasciculations Nerve conduction studies Serum protein electrophoresis Muscle biopsy MRI - so assess for other key differentials
41
What is Kennedy disease?
X linked spinobulbar muscular atrophy Associated with a CAG trinucleotide repeat mutation Lower motor neurone disease Causes progressive weakness and wasting of the limb and bulbar muscles with an absence of spasticity and slight sensory neuropathy Associated with gynaecomastia and reduced fertility
42
Causes of generalised wasting of hand muscles
Anterior horn cell - MND - syringomelia - cervical cord compression - polio Brachial plexus - cervical rib - Pancoast’s tumour - trauma Peripheral nerve - combined median and ulnar nerve lesion - peripheral neuropathy Muscle - disuse atrophy
43
What are Fasciculations?
Caused by axonal loss resulting in the surviving axons recruiting and innerating more myofibrils than usual resulting in large motor units Seen commonly in MND and syringomelia
44
Clinical signs of myelopathy
UMN signs: hypertonia, ankle clonus, generalised weakness, hyperreflexia with up going plantars, hyperreflexia
45
How to differentiate cause of myelopathy
Sensory level which might suggest where the lesion is Scars or spinal deformity Signs of MS Bladder symptoms/catheter Suggest testing anal tone
46
Causes of myelopathy
MS Spinal cord compression Trauma MND Anterior spinal cord thrombosis Syringomelia Hereditary spastic paraplegia Subacute combined degeneration of the cord (absent reflexes with upgoing plantars)
47
Lower limb myotomes
Hip flexion - L2/3 Knee extension - L3/4 Foot dorsiflexion- L4/5 Knee flexion - L5/S1 Foot plantarflexion - S1/2
48
What are the key features of Kennedy disease?
Slow progression Perioral Fasciculations Associated with gynaecomastia and reduced fertility
49
How does poliomyelitis present?
Acute flaccid paralysis, typically unilateral. Reduced reflexes and atrophy of the affected limb. GI prodrome.
50
What is post- poliomyelitis syndrome?
Weakness, fatigue and wasting of affecting muscles
51
How does GBS present?
Flaccid paralysis Hyporeflexia Ascending weakness Variable sensory loss
52
Differential diagnosis for GBS?
CIDP if more chronic onset of symptoms
53
Investigations for GBS
CSF: normal wcc and glucose with raised protein NCS: delayed conduction velocities indicating demyelination of peripheral nerves Spirometry to monitor FVC
54
Treatment of GBS
IVIG and plasma exchange Nutritional support Ventilatory support Pressure care Analgesia
55
Causes of spastic paraparesis
Group based on onset time: Hyper acute- vascular (less likely to spastic, more likely spastic shock) Acute - spinal cord compression, transverse myelitis Gradual onset - subacute combined degeneration of the cord, Frederichs ataxia, hereditary spastic paraparesis
56
Investigating spastic paraparesis
MRI spine Check b12, copper
57
Clinical signs of spastic paparesis
Wheelchair/ walking aides Increased tone and ankle clonus Generalised weakness Hyper- reflexia and extensor plantars Scissoring gait Signs to look for cause: Assess for sensory level Check back for scars or deformity MS signs Anal tone
58
Clinical presentation of Parkinson’s
Bradykinesia Cogwheel rigidity Resting pill rolling tremor Shuffling gait Postural instability Mask like facies Reduced blink frequency Dysphasia Micrographia Hypophonia Freezing Depression Fatigue Sleep disturbance Cognitive impairement Anosmia
59
Signs and symptoms more consistent with Parkinson’s disease
Unilateral onset and persistent asymmetry Resting tremor Good response to levodopa Long disease course
60
Differential diagnosis for Parkinsonism
Drug induced Vascular Dementia with Lewy bodies Multiple system atrophy Progressive supranuclear palsy
61
Signs/ symptoms consistent with multiple system atrophy
Prominent early autonomic features (postural hypotension, urinary incontinence, erectile dysfunction) Cerebellar signs Prominent pyramidal signs Poor levodopa response
62
Sighs and symptoms consistent with progressive supranuclear palsy
Vertical supranuclear gaze palsy Early falls (within first year) Poor levodopa response Early dementia
63
What is the aetiology of Parkinson’s disease?
Early onset Parkinson’s is associated with mutation of the PARK-1 gene encoding alpha synuclein Around 20% of cases of Parkinson’s have a first degree relative affected
64
What medications can cause Parkinsonism?
Antipsychotic drugs Metoclopramide Prochlorperazine Sodium valproate Lithium
65
How is Parkinson’s diagnosed?
Clinical diagnosis - if at least 2/4 clinical signs SPECT CT/MRI to rule out alternative causes
66
Management of Parkinson’s disease
1) Levodopa + dopa decarboxylase inhibitor 2) Dopamine agonist (eg. Pramipexole, ropinirole, rotigotine) 3) MAO-B inhibitors (selegiline) 4) COMT inhibitors (eg. Entacapone) DBS
67
Pathology of Parkinson’s disease
Degeneration of the dopaminergic neurones between the substantia nigra and basal ganglia
68
Differential diagnosis for tremor
Resting tremor: Parkinson’s Postural tremor: benign essential tremor, anxiety, thyrotoxicosis, co2, hepatic, alcohol Intention tremor: cerebellar disease
69
Causes of ischaemic stroke
Thrombotic, most commonly caused by atherosclerosis Embolic, most common in patients with AF, but also valve defects or endocarditis
70
Causes of haemorrhagic stroke
Intracranial haemorrhage most commonly secondary to uncontrolled hypertension SAH secondary to AV malformations or Berry aneurysms
71
Risk factors for stroke
Hypertension DM Hypercholesterolaemia AF IE Carotid artery disease CCF congenital/structural heart disease Age Genetics Gender Sickle cell disease Antiphospholipid syndrome CKD Smoking Alcohol
72
What is the Pathophysiology of ischaemic stroke
Acute occlusion of an intracranial vessel leads to reduced blood flow to the brain region supplied by the vessel resulting in infarction via 2 pathways: 1. Necrotic pathway with rapid cytoskeletal breakdown 2. Apoptotic pathway
73
Bamford classification of stroke
TACS- contralateral hemiplegia, homonomous hemianopia, higher cortical dysfunction (ie. Aphasia, dyspraxia, neglect) PACS- 2/3 of the above LACS- pure hemi- motor/sensory loss POCS- cranial nerve impairement, unilateral or bilateral sensory/motor impairment, disorder of conjugate eye movement, cerebellar dysfunction, homonymous hemianopia, cortical blindness
74
Management of suspected stroke
History+ collateral (onset time, functional baseline) Examination BM ECG CT head +/-CT perfusion MRI Echo Carotid doppler Clotting screen and vasculitis screen if young
75
Management of ischaemic stroke
<4.5 hours from symptoms onset- thrombolyse with alteplase, start aspirin 24 hrs after thrombolysis If cannot thrombolyse consider perfusion imaging +/- thromboectomy If not able to do the above then 300mg aspirin as a stat and continue for 2 weeks, then long term clopidogrel
76
Management of haemorrhagic stroke
Control BP Neurosurgical discussion
77
Management of TIA
Aspirin 300mg stat and continue for 2 weeks then clopi. Start statin immediately Stroke review within 24 hours If crescendo TIA, ongoing neurological symptoms, severe cardiac stenosis or suspected cardio- Embolic cause they need admission
78
When is a decompressive hemicraniectomy considered in stroke?
Clinical deficits which suggest an infarct in the middle cerebral artery with a NIHSS score of > 15, decreased consciousness, signs on CT of an infarct of at least 50% of the middle cerebral artery territory
79
MRC power grade
0- none 1- flicker 2- moves with gravity neutralised 3- moves against gravity 4. Reduced power against resistance 5. Normal
80
Common triggers for migraine
Stress Menstruation Fasting/missed meals Caffeine Irregular sleep pattern
81
Risk factors for developing chronic migraine
Sleep disorders Excessive use of anti- migraine medication Emotional stress Obesity Increased episodic migraine attacks Anxiety/depression Head injury
82
Clinical presentation of migraine
Unilateral pulsation headache Photophobia N&V Zigzags, scotoma or flashing lights in vision Increased sense of smell Dizziness Pins and needles Prodrome and postdrome
83
Important points to examine in headache history
Fundoscopy Eye movements (palsy and nystagmus) Visual fields Cerebellar signs Localising signs
84
Red flag symptoms for headache
Sudden onset New and persistent headache Age >50 Early morning headache Postural symptoms Fevers/rash/neck stiffness/photophobia
85
Management of migraine
Education Avoid analgesia over use Stop COCP Simple analgesia Triptans Antiemetic Prophylaxis- propranolol, topiramate, amitriptyline
86
Investigating polyneuropathy
FBC B12 Fasting glucose/HbA1c LFTs U&Es TFTS Serum immunoglobulins and electrophoresis NCS EMG CT/MRI/ nerve biopsy
87
What is the aetiology of Huntington’s disease?
Caused by mutations in the Huntington gene on chromosome 4 encoding a CAG- repeat expansion within the gene. It has the genetic characteristics of complete penetrance and anticipation whereby earlier age of onset occurs in later generations due to expansion of the CAG repeat
88
Clinical presentation of Huntingtons
- prodrome of mild psychotic and behavioural symptoms - chorea - slow saccadic eye movements - psychosis - depression - irritability - dementia
89
Differential diagnosis for chorea
Huntington’s SLE Wilson’s Stroke (asymmetrical) Hypoglycaemia Polycythaemia Sydenham’s chorea (group a beta haemolytic strep)
90
Diagnosis of Huntingtons
FHx (inc. missed diagnosis ie. Psychiatric illness) MRI shows changed in mod-severe disease Genetic testing Testing for alternative cause
91
Management of Huntingtons
MDT Neurologist Neuropsychologist Dietitian (increased BMR) Occupational and physical therapists
92
What causes myasthenia gravis?
Acquired autoimmune condition caused by autoantibodies against post-synaptic neuromuscular junction receptors
93
How does myasthenia gravis present?
Fatiguable weakness Ptosis Diplopia Proximal weakness Loss of facial expression Dysarthria Dysphagia Slurred speech Dysphonia
94
How would you investigate myasthenia gravis?
Anti- AChr antibodies in 90% of cases Anti- MuSK (muscle specific kinase) antibodies in 10% of cases particularly Afro Caribbean EMG: decremented response to a titanic train of impulses and EMG jitter Tensilon test - less used now due to risk of cardiac arrest (have arrest trolley and atropine ready) CT mediastinum to look for thymoma TFTS (Graves present in 5% of cases) Spirometry Assess for infection in myasthenia crisis
95
Treatment of myasthenia crisis
Spirometry Screen for infection Critical care input if: - FVC <20ml/kg - progressive decline in FVC - can’t manage secretions - sniff nasal insp pressure <40 - can’t complete sentences or lift head off pillow IVIg and plasmapheresis
96
Treatment of myasthenia gravis
Sussman protocol (steroids and pyridostigmine) Steroids- uptitrating, at risk of steroid dip, if significant symptoms they need inpatient monitoring Pyridostigmine (cholinesterase inhibitor) Steroid sparing agents (MMF, aza, ect.) Thymectomy
97
What is Lambert- Eaton myasthenic syndrome?
Diminished reflexes that become brisker after exercise Lower limb girdle weakness Associated with malignancy eg. Small cell lung cancer Antibodies block pre-synaptic calcium channels EMG shows a second wind phenomenon on repetitive stimulus
98
How does Fredereich’s ataxia present?
Young adult Wheelchair Ataxic gait Pes cavus Bilateral cerebellar ataxia Leg wasting with bilateral upgoing plantars and absent reflexes Posterior column signs ( loss of vibration and joint position sense) Kyphoscoliosis HOCM Optic atrophy Hearing loss
99
What causes Fredreich’s ataxia?
Autosomal recessive Defect in the FXN gene which carries the code for the frataxin protein GAA repeat expansion Mutations cause oxidative injury associated with excessive iron deposits in the mitochondria
100
How would you investigate someone with suspected Friedreich’s ataxia?
NCS Genetic analysis ECG Exclude vitamin E deficiency MRI - atrophy changes
101
Treatment of Friedreichs ataxia
MDT Physio SALT OT Monitor cardiac function
102
What are the clinical signs of dystrophia myotonica?
Myopathic facies Wasting of facial muscles and SCM Bilateral ptosis Frontal balding Dysarthria Percussion myotonia- percuss thenar eminence and watch for involuntary thumb flexion Cataracts Cardiomyopathy Diabetes Testicular atrophy Dysphagia
103
What causes dystrophia myotonica?
Type 1: expansion of CTG trinucleotide repeat sequence within DMPK gene on chromosome 19 Type 2: expansion of CCTG tetranucleotide repeat sequence within ZNF9 gene on chromosome 3 Autosomal dominant Genetic anticipation present
104
How is dystrophia myotonica diagnosed?
Clinical features EMG: Dive-bomber potentials Genetic testing
105
How is dystrophia myotonica managed?
Phenytoin may help myotonia Advice against GA MDT
106
Causes of ptosis
Bilateral - myotonic dystrophy, MG, congenital Unilateral - third nerve palsy, horners syndrome
107
How does syringomelia present?
Weakness and wasting of small muscles of the hand Loss of reflexes in upper limbs Loss of pain and temperature with preservation of position and vibration sense Charcot joints Pyramidal weakness in lower limbs with upgoing plantars Kyphscoliosis Hornets syndrome
108
What causes syringomelia?
Progressively expanding fluid filled cavity within the cervical cord - causes LMN weakness at level of syrinx with loss of pain and temp sensation and UMN weakness below the level of the syrinx
109
What is a Charcot joint?
Painless deformity and destruction of a joint with new bone formation following repeated minor trauma secondary to loss of pain sensation
110
Causes of Charcot joint
Tabes dorsalis- hip and knee Diabetes - foot and ankle Syringomelia - elbow and shoulder
111
How does facial nerve palsy present
Unilateral facial droop Absent nasolabial fold and forehead creases Bell’s phenomenon: eyeballs roll upwards in attempted eye closure
112
Locating level of the lesion causes facial nerve palsy
Pons (MS/stroke) + 6th nerve palsy and long tract signs Cerebellar- pontine angle (acoustic neuroma) + 5th,6th,8th palsy + cerebellar signs Auditory/facial canal (cholesteatoma or abscess) + 8th nerve palsy Neck and face - scars or parotid mass
113
Management of Bells Palsy
Steroids Eye protection Aciclovir if severe
114
Clinical signs of tuberous sclerosis
Adenoma sebaceum in butterfly distribution Periungual fibroma Shagreen patch Ash leaf macules Cystic lung disease Renal enlargement Transplanted kidney/evidence of dialysis Retinal phakomas Seizures Signs of anti-epileptic therapy
115
Genetics of tuberous sclerosis
Autosomal dominant Type 1- chromosome 9 Type 2 - chromosome 16
116
Renal manifestations of tuberous sclerosis
Renal angiomyolipomas, renal cysts and RCC
117
Investigating tuberous sclerosis
Skull films show railroad tract calcification CT/MRI head showing tuberous masses in the cerebral cortex Echo and US abdo show hamartomas and renal cysts
118
Clinical signs of neurofibromatosis
Cutaneous neurofibromas Cafe au lait patches Axillary freckles Lisch nodules Hypertension Honeycomb lung/fibrosis Palpable enlarged nerves Poor visual acuity due to optic glioma/compression
119
Clinical signs of Horner’s pupil
Ptosis Enophthalmos (sunken eye) Anhydrosis Miosis (small pupil) Look at the ipsilateral side of the neck for scars and tumours (Pancoast’s)
120
Causes of Horner’s pupil
MS Stroke (Wallenberg) Syrinx Aneurysm Trama Pancoast’s
121
Clinical signs of a Holmes-Adie pupil
Moderately dilated pupil that had a poor response to light and a sluggish response to accommodation Absent or diminished ankle and knee jerks This is a benign condition more common in females. Provide reassurance.
122
Clinical signs of an Argyll Robinson pupil
Small irregular pupil, accommodates but doesn’t react to light. Atrophied and depigmented iris. Look for sensory ataxia (tabes dorsalis)
123
Causes of Argyll Robertson pupil
Syphilis - tabes dorsalis - demyelination predominantly in dorsal root ganglia - will also have sensory ataxia and pain - test using TPHA or FTA - treat with penicillin Diabetes
124
Clinical signs of a 3rd nerve palsy
Ptosis, usually complete Dilated pupil Eye points down and out On looking nasally the eye will intort suggesting normal trochlear nerve function
125
Causes of a 3rd nerve palsy
Medical: - mononeuritis multiplex - midbrain infarct (Weber’s) - MS - Migraine Surgical: - Posterior communicated artery aneurysm - cavernous sinus pathology - cerebral uncus herniation
126
How does optic atrophy present?
Relative afferent pupillary defect: dilation of the pupil on moving the slight source from the normal eye (consensual reflex) to the abnormal eye (direct reflex)- also known as Marcus Gunn pupil Disc pallor on fundoscopy
127
Causes of optic atrophy
MS Friedreichs ataxia Paget’s disease