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Y4 special senses, neurology & dermatology > Neurology conditions > Flashcards

Neurology conditions Flashcards

1
Q

Seizure

A

uncontrolled discharge of neurons within the CNS

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2
Q

Prodrome

A

mood/behavioural changes that occur before a seizure

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3
Q

Aura

A

symptom immediately before the seizure, helps to localise

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4
Q

Postictal period

A

period of time immediately after the seizure

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5
Q

Partial seizure

A
  • partial - one specific location of the brain, often lobe
    • frontal lobe = jacksonian march → involuntary movement of one muscle group to the neck (up the arm)
    • parietal lobe = sensory disturbance in extremities or in the face
    • temporal lobe = visceral disturbance, memory disturbance, motor disturbance & affective disturbance
    • occipital lobe = visual hallucination before the seizure
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6
Q

Generalised seizure

A
  • generalised = affect both hemispheres
    • absence = pt stares vacantly
    • myoclonic = sudden brief generalised muscle contractions
    • tonic = sudden, sustained muscular contraction
    • atonic = loss of muscle tone & sudden fall
    • tonic-clonic = combination of tonic, followed by a clonic phase
      • partial seizure can develop into tonic clonic seizure
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7
Q

Epilepsy syndromes

A

West syndrome (4-6 months) - salaam attacks, hypsarrhythmias (EEG)

Lennox-Gaustat (1-3 years) - drop attacks, LD

Childhood absence epilepsy - staring blankly, no recollection

Juvenile myoclonic syndrome - throwing drinks or food in the morning, characteristic EEG

Sturge Weber syndrome - port wine stain in region of trigeminal nerve

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8
Q

Epilepsy ix

A

Neuroimaging

EEG

ECG

Additional = blood tests

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9
Q

Epilepsy mx

A

Generalised seizures = 1st line is sodium valproate OR

  • TC, tonic, atonic = lamotrigine
  • absence = ethosuximide
  • myoclonic = levetiracetam

Focal seizures = 1st line is lamotrigine OR carbamazepine

  • 2nd line = levetiracetam OR oxcarbazepine OR sodium valproate

Driving advice

  • 1st seizure = 6 months off if no relevant structural abnormalities, 1 year if this not met
  • epilepsy & medication = 1 year free of attacks
  • epilepsy without medication = 6 months free of attacks
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10
Q

Migraine

A

Recurrent moderate to severe headache commonly associated with nausea, vomiting, photophobia & phonophobia

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11
Q

Migraine clinical features

A

Headache - unilateral, pulsating, moderate/severe pain intensity, N&V, photophobia, phonophobia

Aura - scintillating scotoma, numbness, tingling, dysphasia

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12
Q

Migraine acute mx

A

Simple analgesia

Triptans - oral sumatriptan

Anti-emetics - buccal prochlorperazine

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13
Q

Migraine prevention

A

Trigger avoidance

Preventative treatment - propranolol, topiramate, amitriptyline

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14
Q

Migraine complications

A

Status migrainosus - debilitating migraine that persists > 72 hours

Persistent aura without infarction - symptoms of aura for > 1 week

Migrainous infarction

Migraine aura-triggered seizure

Ischaemic stroke

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15
Q

IIH

A

Disorder characterised by chronically elevated intracranial pressure

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16
Q

IIH risk factors

A

Overweight & obese

Females

Reproductive age

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17
Q

IIH clinical features

A

Clinical features of raised ICP

Headache - worse on lying down or bending over

Transient visual loss

Photopsia

Tinnitus (pulsatile)

Diplopia

Visual loss

Other features - neck, back and/or retrobulbar pain

Signs - papilloedema, visual loss, 6th nerve palsy

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18
Q

IIH ix

A

Basic - obs, urinalysis, bloods, ophthalmoscopy

Neuroimaging - MRI, CT

LP - >25cm H20 consistent with IIH

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19
Q

IIH mx

A

Weight loss

Serial LP

Pharmacotherapy - carbonic anhydrase inhibitor (acetazolamide)

  • other meds: topiramate, furosemide

Surgical treatment - optic nerve sheath fenestration OR shunting

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20
Q

Cluster headache

A

Severe primary headache disorder characterised by recurrent unilateral headaches centred on the eye/temporal region

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21
Q

Cluster headache clinical features

A

Very severe unilateral orbital/supraorbital and/or temporal pain

Conjunctival infection and/or lacrimation

Nasal congestion

Eyelid oedema

Forehead and facial sweating

Miosis and/or ptosis

Sense of restlessness or agitation

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22
Q

Cluster headache ix

A

Neurology referral

MRI brain

CT head

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23
Q

Cluster headache mx

A

Trigger avoidance

Acute management

  • triptans - subcut/intranasal route
  • short burst oxygen therapy

Preventative management

  • verapamil
  • other options - glucocorticoids, lithium

Refractory disease

  • greater occipital nerve blocks
  • deep brain stimulation
  • trigeminal nerve compression
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24
Q

Trigeminal neuralgia

A

Chronic pain condition characterised by severe, sudden & brief bouts of shooting/stabbing pain that follow distribution of one/more divisions of the trigeminal nerve

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25
Q

Trigeminal neuralgia aetiology

A

Idiopathic

Malignancy

AV malformation

MS

Sarcoidosis

Lyme disease

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26
Q

Trigeminal neuralgia clinical features

A

Unilateral facial pain that is sudden, severe & brief

  • shooting and stabbing

Triggers = touch, eating, wind blowing, cold

Examination is normal

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27
Q

Trigeminal neuralgia ix

A

Clinical diagnosis

MRI - exclude secondary causes

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28
Q

Trigeminal neuralgia mx

A

Medical - carbamazepine

  • other options: phenytoin, lamotrigine, gabapentin

Surgical - microvascular decompression, treatment of underlying cause, alcohol/glycerol injections

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29
Q

Medication overuse headache

A

Present for 15 days or more per month

Developed or worsened whilst taking regular symptomatic medication - down-regulation of pain receptors

Patients using opioids & triptans are at most risk

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30
Q

Medication overuse headache mx

A

Withdraw offending drugs

Consider restarting previously used drugs at a lower dose or different drugs not previously used

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31
Q

Temporal arteritis (also called GCA)

A

Condition where the arteries, particularly the temples, become inflamed

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32
Q

Temporal arteritis clinical features

A

Temporal headache - GCA can cause blindness & stroke

Jaw claudication

Amaurosis fugax (transient monocular blindness, often described as a dark curtain descending vertically)

Systemic features - fatigue, fevers, weight loss & malaise

GCA & PR often occur together

O/E - thickened, tender temporal artery, scalp tenderness

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33
Q

Temporal arteritis ix

A

Bloods - inflammatory markers, FBC & LFTs

Temporal artery biopsy - granulomatous inflammation of the inner half of the media with infiltration of inflammatory cells

Doppler ultrasonography - ‘halo sign’

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34
Q

Temporal arteritis mx

A

High-dose steroids immediately

Gradual taper steroids over 1-2 years

Steroid protection - bisphosphonates & PPIs

Low dose aspirin - further reduce the risk of stroke & blindness

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35
Q

Tension headaches clinical features

A

Bilateral, non-pulsatile headaches

Tightness sensation (like band around the head)

Scalp muscle tenderness

Associated with stress, depression, alcohol, skipping meals, dehydration

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36
Q

Tension headaches mx

A

Reassurance

Analgesia per the WHO pain ladder

Amitriptyline is generally first-line chronic/frequent tension headaches

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37
Q

Idiopathic Parkinson’s Disease and Parkinsonism

A

Chronic, progressive neurodegenerative condition resulting from the loss of dopamine-containing cells of the substantia nigra

Parkinsonism = umbrella term for the clinical syndrome involving bradykinesia & at least one of tremor, rigidity and/or postural instability

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38
Q

PD pathophysiology

A

Loss of dopaminergic neurons in the substantia nigra & development of Lewy bodies (a-synuclein)

LRRK2 mutations most common type in familial & sporadic PD

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39
Q

PD clinical features

A

Triad - rigidity, bradykinesia & tremor

Shuffling gait - impaired balance on turning, flexed posture giving stooped appearance, reduced arm swing, short stride length

Hypophonia, micrographia, pseudohypersalivation, hypomimia

Non-motor symptoms: anosmia, low mood, anxiety, constipation, REM sleep disorder, fatigue

O/E:

  • tremor - worse at rest, pill-rolling, re-emergent tremor with posturing, 4-6 Hz
  • bradykinesia - reduced/slow movement & difficult initiation of movement, reduced arm swing, reduction in amplitude with repetitive movements
  • rigidity - increase resistance to passive movement, cogwheel due to superimposed tremor
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40
Q

PD clinical rating scales

A

Heohn and Yahr scale

UPDRS

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41
Q

PD ix

A

Clinical diagnosis

Neuroimaging (CT/MRI) - strong suspicion of a secondary cause/failed response to treatment

DaTSCAN (type of SPECT imaging) - differentiate Parkinsonism from essential tremor

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42
Q

PD mx

A

Treatments mainly work by increasing dopamine levels

Initial management:

  • Levodopa - most improvement in motor symptoms
    • more likely to get dyskinesia later down the line
  • Dopamine agonists
    • more specified adverse events (excessive sleepiness, hallucinations & impulse control disorders)
  • MAO-B inhibitors - less effective than first two meds

Adjuvant treatment:

  • COMT inhibitors - inhibit the peripheral breakdown by the COMT enzyme → more levodopa to cross the blood brain barrier
  • anti-muscarinics, amantadine, apomorphine

Surgical management:

  • deep brain stimulation
  • specialist centres → thalamic/subthalamic surgery

MDT input - OT, physios, dieticians

Drugs to avoid:

  • flupentixol
  • haloperidol
  • chlorpromazine
  • prochlorperazine
  • metaclopramide
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43
Q

PD complications

A

Motor:

  • motor fluctuations
  • dyskinesia
  • freezing of gait
  • ‘wearing off’ phenomenon
  • falls

Non-motor complications:

  • aspiration pneumonia
  • bladder, bowel and sexual dysfunction
  • pressure sores
  • impulse control disorders & psychosis
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44
Q

Parkinsonism differentials

A

Vascular

Drug-induced - anti-psychotics

Benign essential tremor - responds to alcohol, 1st line treatment is propranolol

Dementia with Lewy bodies - presence of parkinsonism & dementia within 1 year

Parkinson plus conditions - progressive supranuclear palsy, multi-system atrophy, dementia with lewy-body, corticobasal degeneration

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45
Q

GBS

A

An acute, inflammatory polyneuropathy typically characterised by a progressive, ascending neuropathy

Refers to a number of ‘variants’ with unique features & pathogenesis → AIDP

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46
Q

GBS triggers

A

Campylobacter jejuni - common cause of food poisoning & gastroenteritis

Other infections - CMV, EBV, hepatitis E & mycoplasma pneumoniae

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47
Q

Acute inflammatory demyelinating polyneuropathy (AIDP)

A

Classical symptoms:

  • progressive symmetrical weakness in limbs
  • reduced or absent tendon reflexes
  • reduced sensation

Symptoms tend to ascend from distal muscles of the limbs

Commonly history of preceding viral illness

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48
Q

Acute motor axonal neuropathy (AMAN)

A

Form of GBS that results from axonal involvement typically following infection with campylobacter

Progresses more rapidly than AIDP & does not demonstrate sensory nerve involvement

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49
Q

Acute motor and sensory axonal neuropathy (AMSAN)

A

Severe form of AMAN that also demonstrates involvement of sensory nerves

Characterised by axonal degeneration of both sensory & peripheral nerves

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50
Q

Miller Fisher syndrome

A

Variant characterised by unique presentation:

  • ataxia
  • areflexia
  • ophthalmoplegia

25% will also develop some weakness in the extremities

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51
Q

GBS ix

A

Bedside - vital signs, blood sugar, pregnancy test (if indicated), stool culture (if indicated), urine porphobilinogen

Bloods - FBC, renal function, LFTs, CRP, bone profile & Mg, HbA1c, thyroid profile, B12/folate/thiamine

Imaging - CXR, MRI spine

Nerve conduction studies, electromyography, LP, antibodies (anti-GQ1b), spirometry

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52
Q

GBS mx

A

Supportive care

  • monitor for respiratory failure
    • 4 hourly FVC is an important component
  • cardiovascular monitoring
  • DVT prophylaxis
  • analgesia

Immunotherapy - speed up recovery

  • IV immunoglobulin
  • plasma exchange - removes circulating antibodies & other immune modulators
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53
Q

GBS clinical course

A

Symptoms develop rapidly over two weeks before plateauing, with recovery around week four

Factors associated with poorer prognosis - old age, preceding campy infection, rapid onset & severe presenting symptoms

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54
Q

MND

A

Clinical syndrome characterised by prominent and progressive muscular weakness

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55
Q

MND risk factors

A

Increasing age

Male

Genetic predisposition

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56
Q

MND phenotype

A

Amyotrophic lateral sclerosis (ALS) - affects both upper and lower motor neurones

Progressive bulbar palsy - primarily affecting bulbar muscles (speech & swallowing)

Primary lateral sclerosis (PLS) - predominately affects UMNs

Progressive muscular atrophy (PMA) - predominantly affects LMNs

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57
Q

MND pathophysiology

A

Progressive degenerative disorder of both upper and lower motor neurones

Sensory neurones are spared

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58
Q

MND genetics

A

TDP-43 → pathological feature

C9orf72 gene - most common genetic abnormality → both loss and gain of function mutations

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59
Q

MND UMN vs LMN signs

A

UMN - hypertonia, pyramidal pattern of weakness, hyperreflexia, positive jaw jerk, slow tongue movements, disuse atrophy, Hoffman’s and extensor plantar responses

LMN - hypotonia, areflexia, wasting, fasciculations

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60
Q

MND clinical presentation

A

Presence of both upper & lower motor neuron signs with an insidious onset

Limb onset

Bulbar phenotype → progressive dysarthria & dysphagia, tongue fasciculations

Triceps & finger flexors are comparatively spared

Wasting of thenar eminence & 1st dorsal interosseous

Hip flexion & ankle dorsiflexion often affected

Cognitive impairment

Overlap with FTD

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61
Q

MND diagnosis

A

Clinical diagnosis

Electromyography - active denervation with compensatory reinnervation

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62
Q

MND ix

A

MRI brain, spine

LP

Bloods

Resp function → can’t ventilate properly

ECG - riluzole can cause tachycardia

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63
Q

MND mx

A

Riluzole (glutamate inhibitor) - can prolong life by approx. 3 months

Supportive/palliative treatment:

  • NIV
  • gastrotomy
  • manage other symptoms eg. spasticity, cramps, head drop
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64
Q

MG

A

Autoimmune disease marked by production of antibodies that target the nicotinic acetylcholine receptors on muscle fibres

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65
Q

MG clinical features

A

Limb muscle weakness

Extra-ocular muscle involvement - drooping eyelids, diplopia

Facial muscle involvement - difficulty in smiling or chewing

Bulbar muscle involvement - change in speech or difficulty swallowing

O/E - fatigable muscle weakness, bilateral ptosis, myasthenic snarl, head droop & bulbar features

Symptoms typically worsen with prolonged movement/by end of the day

66
Q

MG ix

A

Ice-pack test

Bloods - serum acetylcholine receptor antibody & muscle-specific tyrosine kinase antibodies

Imaging investigations - CT scan of the chest to identify thymic hyperplasia/thymoma

Nerve conduction studies/EMG

Myasthenic crisis → serial pulmonary function tests

67
Q

MG mx

A

R/w in neurology, MDT

Medical management - steroids, anticholinesterase inhibitors (pyridostigmine)

Acute cases - IVIG or plasmapheresis

Surgical management with thymectomy → in patients with thymic hyperplasia/thymoma

68
Q

Spinal muscular atrophy

A

Inherited disease that affects LMN

Autosomal recessive defect in SMN1 gene

Hypotonia, areflexia, poor feeding, not meeting milestones, respiratory failure

69
Q

MS

A

Relapsing-remitting MS (most common) - unpredictable attacks which may or may not leave permanent deficits followed by periods of remission

Neuroinflammatory disorder characterised by demyelination of the central nervous system

69
Q

MS classification

A

Mcdonald’s criteria (2017) - classification of MS

  • dissemination in space
  • dissemination in time
70
Q

MS risk factors

A

F>M

Age (<50)

Genetics

Geographical distribution

Infections

71
Q

MS aetiology

A

Multiple genes

EBV

Low vitamin D

Smoking

Obesity

72
Q

MS presentation

A

Unilateral optic neuritis - demyelination of the optic nerve & presents with unilateral reduced vision, developing over hours to days

  • central scotoma (enlarged central blind spot)
  • pain with eye movement
  • impaired colour vision
  • relative afferent pupillary defect - pupil in the affected eye constricts more when shining a light in the contralateral eye than when shining in the affected eye

Painless binocular diplopia

Focal brainstem/cerebellar syndrome

Partial transverse myelitis with sensory and/or motor symptoms

Examination - focus on eye examination (check vision, light perception, extraocular movements)

73
Q

MS ix

A

Obs

Bloods

MRI brain (gold standard for diagnosis)

LP - CSF will show oligoclonal bands

74
Q

MS mx

A

Acute treatments - steroids (5 days of IV methylprednisolone) → makes attack shorter, improves recovery, minimises risk of permanent symptoms

Chronic treatments - disease modifying therapies

MDT approach

75
Q

Polyneuropathy

A

Refers to damage or dysfunction of multiple nerves of the peripheral nervous system

Typically lead to symmetrical involvement of distal peripheral nerves in a ‘length-dependent’ manner → meaning the longer nerves of the legs & arms are affected first

76
Q

Polyneuropathy classification (onset)

A

Acute - rapid progression from onset to worst clinical features within 4 weeks

  • eg. GBS, vasculitis, certain toxins or critical illness

Chronic

  • eg. diabetes mellitus, CKD, hereditary neuropathies, alcohol excess
77
Q

Polyneuropathy classification (pathology)

A

Demyelination - refers to damage to the myelin sheath that insulates nerves & improves conduction

  • eg. autoimmune diseases, hereditary causes or myeloma

Axonal degeneration - refers to damage to the nerve axon that extends from the cell body & transmits electrical conduction

  • eg. systemic diseases → diabetes mellitus, connective tissue disease, vitamin B12 deficiency
78
Q

Polyneuropathy classification (clinical presentation)

A

Motor - refers to damage/dysfunction of motor nerves

  • weakness & atrophy of affected muscles
  • eg. chronic demyelinating inflammatory polyneuropathy, GBS & Charcot-Marie-Tooth

Sensory - damage or dysfunction of sensory nerves

  • may be ‘negative’ referring to loss of normal sensation eg. touch, proprioception or vibration
  • may be ‘positive’ referring to dysregulated function eg. pain, paraesthesia or burning
    • diabetes mellitus, alcohol excess, CKD, paraneoplastic syndromes
79
Q

Polyneuropathy classification (small and large fibre)

A

Large fibres - carry information to control movement & important sensory information

  • touch, vibration & proprioception

Small fibres - carry information about pain & temperature → painful polyneuropathies

80
Q

Polyneuropathy aetiology

A

Idiopathic

Diabetes mellitus

Systemic illness - CKD, chronic liver disease, amyloidosis

Autoimmune - GBS

Inflammatory - CIDP

Toxic - alcohol, chemo, heavy metals

Neoplastic - myeloma, paraneoplastic syndrome

Hereditary - Charcot-Marie-Tooth

Nutritional - vitamin B12, folate, pyridoxine, vit E deficiencies

Vasculitis

Medications

81
Q

Polyneuropathy - diabetes mellitus

A

Most common cause of polyneuropathy

Can cause a wide range of peripheral neuropathies:

  • distal, symmetrical polyneuropathy
  • autonomic neuropathy
  • radiculopathies
  • mononeuropathies
  • mononeuritis multiplex

Nerve damage occurs due to oxidative stress as part of a byproduct of different metabolic pathways that occur due to persistent hyperglycaemia

82
Q

Polyneuropathy - charcot-marie-tooth

A

Refers to a collection of peripheral neuropathies due to an inherited mutation

Slowly progressive lower limb neurological changes

  • distal calf atrophy
  • pes cavus
  • clumsy walking
  • weakness
  • reduced sensation

Family history of lower limb abnormalities

Examples: CMT1A, CMT2A

83
Q

Polyneuropathy pathophysiology

A

Demyelination - degeneration of the myelin sheath is seen

Axonal degeneration - damage to nerve axons, typically a symmetrical polyneuropathy with weakness

84
Q

Polyneuropathy clinical features

A

Symmetrical, ‘length-dependent’ neuropathy in a ‘glove and stocking’ distribution

Paraesthesia, sensory loss and/or weakness

Sensory features - burning sensation, paraesthesia, sensory loss, ataxia, loss of light touch, loss of vibration, loss of proprioception

Motor features - weakness, reduced/absent reflexes, hypotonia, fasciculations, muscle atrophy, muscle cramping, deformity

85
Q

Polyneuropathy ix

A

Bloods test - FBC, U&Es, LFTs, vitamin B12, folate, vit E, myeloma screen

Electrodiagnostic tests:

  • electromyography - refers to an assessment of the electrical activity of muscles
  • nerve conduction studies - refers to an assessment of individual peripheral nerve function
    • can determine the type of injury
86
Q

Polyneuropathy mx

A

Treat the underlying cause - avoidance of precipitating drug/toxin, targeted treatments

Manage the symptoms - neuromodulating drugs such as gabapentin/duloxetine

87
Q

Cervical spondylosis

A

Degeneration of the vertebral column in the cervical region

88
Q

Cervical spondylosis risk factors

A

Ageing

Occupation which involves repetitive neck movement/overhead work (eg. painting/decorating)

Previous traumatic neck injury

FHx

89
Q

Cervical spondylosis clinical features

A

Pain and/or stiffness in cervical region

Referred pain: retro-orbital, temporal, occipital, interscapular, upper limbs

O/E:

  • reduced range of movement of neck (all directions)
  • poorly localised tenderness
  • radiculopathy (most common - C5-C7): unilateral neck, shoulder/arm pain, paraesthesia/hyperaesthesia, diminished arm reflexes
90
Q

Cervical spondylosis ix

A

Clinical diagnosis

Cervical XR - osteophyte formation, narrowed disc spaces, narrowing of intervertebral foramina

MRI

91
Q

Cervical spondylosis mx

A

Lifestyle - postural advice, maintain normal activities, avoid use of neck collar

Pharmacological - analgesia, specialist pain clinic, epidural injection

Physiotherapy - symptoms > 4 weeks

OT/psychologist

Surgical - decompressive surgical procedures

92
Q

Cervical spondylosis complications

A

Neurological - radiculopathy & myelopathy

Surgical complications - reduced ROM, accelerated progression of degeneration of adjacent levels

93
Q

Bell’s palsy

A

Unilateral facial nerve palsy of unknown cause

Thought to be related to inflammation and oedema of the facial nerve secondary to a viral infection/autoimmunity

94
Q

Bell’s palsy clinical features

A

Rapid onset (< 72 hours) of unilateral facial weakness

Post-auricular/ear pain

Difficulty chewing

Incomplete eye closure

Drooling

Tingling

Hyperacusis (weakness of the stapedius muscle)

Signs - loss of nasolabial fold, drooping of the eyebrow, drooping of the corner of the mouth, asymmetrical smile, Bell’s sign (upward movement of the eye maintained on attempt to close the eye)

95
Q

Bell’s palsy ix

A

Clinical diagnosis - unilateral facial weakness of rapid onset without forehead sparing

Routine blood tests

Neuroimaging

Specialist tests - LP, lyme serology

96
Q

Bell’s palsy mx

A

Largely supportive but prednisolone may be used in those presenting within 72 hours of onset

General points - patients should be reassured that the prognosis is good, but can take several months to recover

Medical therapy - in patients presenting within 72 hours, prednisolone may be given; anti-viral treatment may be considered

Eye care - critical to provide good eye care with includes drops, advice on taping the eye when sleeping, sunglasses outdoors

  • incomplete eye closure = referred to ophthalmology
97
Q

Bell’s palsy complications

A

Majority make a full recovery within four months

Eye symptoms - corneal ulcer

No improvement after three weeks/develop late problems with aberrant reinnervation

  • voluntary muscle contraction leading to involuntary contraction of another muscle
98
Q

Carpal tunnel syndrome

A

Median nerve neuropathy due to compression as it passes through the carpal tunnel in the wrist

Most common upper limb mononeuropathy

99
Q

Carpal tunnel syndrome risk factors

A

Females

Diabetes

Osteoarthritis

Obesity

Hypothyroidism

Pregnancy

Trauma

100
Q

Carpal tunnel syndrome clinical features

A

Symptoms - pain, paraesthesia, weakness, clumsiness, difficulty with tasks, sensory loss

Signs - sensory loss, thenar eminence wasting, weak thumb abduction & opposition

Positive Phalen’s & Tinel’s test

101
Q

Carpal tunnel syndrome ix

A

Usually clinical

Electromyography

Nerve conduction studies

Imaging reserved for patients with a suspected structural abnormality

102
Q

Carpal tunnel syndrome mx

A

Non-surgical - wrist splints, physical therapy and/or corticosteroids

Surgical - surgical decompression: open carpal tunnel release, endoscopic carpal tunnel release, US guided minimally-invasive release

  • complications
    • wound infection
    • scar formation
    • vascular injury
    • nerve injury
    • complex region pain syndrome
103
Q

Ulnar nerve palsy aetiology

A

Direct trauma/injury to the nerve

Compression/entrapment - cubital tunnel syndrome/Guyon’s canal syndrome

Iatrogenic

Systemic diseases that affect peripheral nerves - DM

104
Q

Ulnar nerve palsy clinical features

A

Weakness or paralysis of most of the intrinsic hand muscles & two muscles in the forearm

Numbness, tingling or pain in sensory distribution of the ulnar nerve (skin of the medial 1.5 digits & associated palm area

105
Q

Ulnar nerve palsy ix

A

Neurological examination

EMG/NCS

MRI/CT scan

106
Q

Ulnar nerve palsy mx

A

Conservative measures - rest, physical therapy, splints

Analgesia

Surgical interventions

107
Q

Radiculopathies

A

Conduction block in the axons of a spinal nerve or its roots, with impact on motor axons causing weakness & on sensory axons causing paraesthesia

108
Q

Radiculopathies aetiology

A

Anything that causes nerve compression

Intervertebral disc collapse

Degenerative diseases of the spine

Fracture

Malignancy

Infection

109
Q

Radiculopathies clinical features

A

Sensory features - paraesthesia & numbness

Motor features - weakness

Radicular pain is often present → burning, deep, strap-like/narrow pain

O/E - important to identify dermatomal & myotomal involvement, ensure to examine for CES

110
Q

Radiculopathies mx

A

Definitive long-term management depends on underlying cause

  • Symptomatic managementAnalgesia - neuropathic pain medications are commonly utilisedAmitriptyline, with pregabalin/gabapentin as alternativesPhysiotherapy
111
Q

Essential tremor

A

Most common type of action tremor that typically involves the hands & is bought out by anti-gravity

Associated with family history & shows an autosomal dominant pattern of inheritance

112
Q

Essential tremor clinical features

A

Characterised by a bilateral kinetic and/or postural tremor of the hands and arms

  • when outstretched or required to perform a specific task

Can affect head & voice

Improves with a small amount of alcohol

Absence of other neurological signs

113
Q

Essential tremor diagnosis

A

Typically based on the following four features:

1) isolated upper limb action tremor

2) with/without tremor in other sites

3) duration > 3 years

4) no other neurological features

114
Q

Essential tremor mx

A

Removing any potential precipitant that makes the tremor worse

  • Pharmacological treatmentPropranololPrimidone - anti-epileptic drug
  • Additional therapiesNeuromodulationBotulinum toxin injectionsDeep brain stimulation
115
Q

Horner’s Syndrome

A

Classic triad of miosis, partial ptosis and anhidrosis

Due to a lesion anywhere along the sympathetic pathway

116
Q

Horner’s Syndrome oculosympathetic pathway

A

Composed of three neurons: first, second & third order

First order neuron (central neuron)

  • fibres travel from the hypothalamus to the spinal cord (C8-T2)

Second order neuron

  • fibres exit the spinal cord via the dorsal roots & enter the sympathetic chain
  • travel upwards over the apex on the lung to the superior cervical ganglion

Third order neuron

  • fibres pass within the adventitia of the internal carotid artery
  • join the ophthalmic portion of the trigeminal nerve at the cavernous sinus & subsequently pass to the pupillary dilator via ciliary nerves
  • post-ganglionic sympathetic fibres innervate a small muscle → ptosis
117
Q

Horner’s Syndrome aetiology

A

First order - lesion anywhere between the brainstem and cervicothoracic spinal cord

  • eg. stroke, SOL, MS, syringomyelia, cervical cord trauma

Second order

  • eg. pancoast tumour, thoracic outlet lesion, trauma, thoracic aneurysm

Third order

  • eg. carotid artery dissection, cavernous sinus pathology, neck mass
118
Q

Horner’s Syndrome mx

A

Neurological emergency = acute, painful Horner’s

Directed towards the underlying cause

Eg. hyperacute stroke unit, thrombolysis, mechanical therapies

119
Q

Subacute combined degeneration of the spinal cord

A

Rare neurological disorder that affects the dorsal columns, lateral corticospinal tracts & spinocerebellar tracts of spinal cord due to vitamin B12 deficiency

120
Q

Subacute combined degeneration of the spinal cord aetiology

A

Vitamin B12 deficiency

  • malabsorption
  • inadequate dietary intake
  • other underlying medical conditions
121
Q

Subacute combined degeneration of the spinal cord clinical features

A

Dorsal column involvement

  • distal tingling/burning/sensory loss is symmetrical & tends to affect the legs more than the arms
  • impaired proprioception & vibration sense

Lateral corticospinal tract involvement

  • muscle weakness, hyperreflexia & spasticity
  • UMN signs typically develop in the legs first
  • brisk knee reflexes
  • absent ankle jerks
  • extensor plantars

Spinocerebellar tract involvement

  • sensory ataxia → gait abnormalities
  • positive Romberg’s sign
122
Q

Subacute combined degeneration of the spinal cord ix

A

Assessment of B12 and folate levels

Homocysteine level analysis - increased level despite normal B12 = functional B12 deficiency

MRI spine

Nerve conduction studies

123
Q

Subacute combined degeneration of the spinal cord mx

A

Vitamin B12 replacement

  • hydroxocobalamin 1mg IM on alternate days until no further improvement
  • maintenance treatment with hydroxocobalamin 1mg IM every two months
124
Q

Cavernous sinus syndromes

A

Constellations of clinical signs and symptoms referable to pathology within or adjacent to the cavernous sinus

125
Q

Cavernous sinus syndromes clinical features

A

Multiple unilateral cranial neuropathies

  • ophthalmoplegia (CN III, IV, VI) - diplopia
  • facial sensory loss (CN V1 and V2)
  • Horner syndrome

Pain

Chemosis

Proptosis

126
Q

Cavernous sinus syndromes aetiology

A

Neoplastic - meningioma, neurofibroma

Inflammatory - sarcoidosis

Infection

Vascular - cavernous malformation, cavernous sinus thrombosis

Traumatic

127
Q

Pituitary tumours classification

A

Adenomas can be classified according to:

  • size (< 1 cm = microadenoma)
  • hormonal status

Prolactinomas are most common types

128
Q

Pituitary tumours clinical features

A

Excess of hormone - Cushing’s disease, acromegaly, galactorrhoea

Depletion of a hormone

Headaches - stretching of dura

Bitemporal hemianopia - compression of optic chiasm

Incidental finding of neuroimaging

129
Q

Pituitary tumours ix

A

Pituitary blood profile - GH, prolactin, ACTH, FSH, LSH, TFTs)

Formal visual field testing

MRI brain with contrast

130
Q

Pituitary tumours mx

A

Medical management:

  • prolactinomas: dopamine agonists (cabergoline or bromocriptine)
  • GH-secreting adenomas: somatostatin analogues & GH receptor antagonists
  • ACTH-secreting adenomas: cortisol synthesis inhibitors

Transsphenoidal surgery

Radiotherapy

131
Q

Wernicke’s encephalopathy

A

Neurological disorder caused by thiamine (vitamin B1) deficiency

132
Q

Wernicke’s encephalopathy aetiology

A

Chronic alcohol abuse

Malnutrition

Bariatric surgery

Hyperemesis gravidarum

133
Q

Wernicke’s encephalopathy clinical features

A

Confusion

Oculomotor abnormalities - gaze-evoked nystagmus, spontaneous upbeat nystagmus & horizontal/vertical ophthalmoplegia

Ataxia (difficulties with coordinated movements)

134
Q

Wernicke’s encephalopathy ix

A

Neurological examination

MRI head

Blood tests - can reveal low thiamine levels

135
Q

Wernicke’s encephalopathy mx

A

High dose IV thiamine (Pabrinex)

136
Q

Wernicke’s encephalopathy complications

A

Permanent horizontal nystagmus

Inability to walk

Deficits in learning & memory

Korsakoff syndrome - irreversible deficits in anterograde and retrograde memory

137
Q

Argyll Robertson pupil

A

Specific finding in neurosyphilis

Constricted pupil that accommodates when focusing on a near object but does not react to light

Often irregularly shaped

138
Q

Creutzfeldt-Jakob Disease (CJD)

A

Neurodegenerative disorder believed to be caused by an abnormal isoform of a cellular glycoprotein - prion

139
Q

CJD classification

A

Sporadic CJD

New variant CJD - younger patients, psychological symptoms are most common presenting features

Other prion diseases - kuru, fatal familial insomnia, Gerstmann Straussler-Scheinker disease

140
Q

CJD clinical features

A

Rapid onset dementia

Neurological symptoms - ataxia, weakness & visual disturbances

Psychiatric impairment - precedes neurological symptoms

Myoclonus

141
Q

CJD ix

A

Diagnosis confirmed by tissue biopsy

Supportive ix:

  • EEG
  • MRI
  • LP
142
Q

CJD mx

A

No cure for CJD

Symptom control

Palliative care

143
Q

Syringomyelia

A

Development of a fluid-filled cyst in the spinal cord

144
Q

Syringomyelia aetiology

A

Chiari malformation

Trauma

Tumours

Idiopathic

145
Q

Syringomyelia clinical features

A

‘cape-like’ (neck and arms) loss of sensation to temperature but preservation of light touch, proprioception & vibration

  • accidentally burn hands without realising

Spastic weakness

Paraesthesia

Neuropathic pain

Upgoing plantars

Bowel & bladder dysfunction

146
Q

Syringomyelia ix

A

Full spine MRI with contrast

Brain MRI - Chiari malformation

147
Q

Syringomyelia mx

A

Directed at treating the cause of the syrinx

Patients with persistent/symptomatic syrinx → shunt into syrinx can be placed

148
Q

Third nerve palsy

A

Neurological condition characterised by weakness or paralysis of the muscles innervated by the CN III

149
Q

Third nerve palsy aetiology

A

Ischaemic (microvascular) third nerve palsy:

  • present without pupillary involvement
  • commonly associated with DM, HTN
  • tend to resolve spontaneously over weeks to months

Compressive (mass lesion) third nerve palsy:

  • typically presents with pupillary involvement
  • can be due to aneurysms, tumours or other SOLs
  • cases require urgent evaluation & management to prevent life-threatening complications
150
Q

Third nerve palsy ix

A

MRI

CTA

151
Q

Third nerve palsy mx

A

Ischaemic CN III palsy:

  • patients should be managed conservatively with observation & control of risk factors
  • spontaneously resolve within a few months

Compressive CN III palsy:

  • urgent evaluation and intervention are required to address underlying cause

Symptom management:

  • patching
  • prism therapy
  • botulinum toxin injections
  • eyelid surgery
152
Q

Facial nerve palsy

A

A condition involvement the unilateral (or sometimes bilateral) dysfunction of the seventh cranial nerve, leading to facial weakness/paralysis

153
Q

Facial nerve palsy aetiology

A

CNS involvement - distinguished due to forehead-sparing weakness (UMN lesion)

Physical lesions of cerebellopontine angle

Basal meningitis

Ramsey Hunt syndrome

Trauma

Diseases of middle/inner ear

Mononeuritis multiplex

154
Q

Facial nerve palsy clinical features

A

Facial weakness or paralysis

Difficulty closing the eye on affected side

Altered sense of taste

Hypersensitivity to sound in one ear

Decreased tearing and salivation

Loss of the nasolabial fold

Drooping of mouth on one side

155
Q

Facial nerve palsy ix

A

Clinical examination & neurological assessment

Imaging - MRI/CT

Serologic tests for Lyme disease/other relevant infectious agents

NCS & EMG → neuromuscular differentials

156
Q

Facial nerve palsy mx

A

Dependent on underlying cause

Bell’s palsy - corticosteroids

RHS - antiviral agents

Lyme disease & basal meningitis - abx

Acoustic neuroma & trauma - surgical intervention

Physical therapy & rehab to restore facial muscle function

Addressing underlying conditions eg. diabetes, htn

157
Q

Sixth nerve palsy

A

Dysfunction of the abducens nerve causing a lateral rectus palsy

158
Q

Sixth nerve palsy aetiology

A

Ischaemia

Neoplastic

Trauma

Cavernous sinus pathology

Deficiency in thiamine & raised ICP - bilateral abducens nerve palsy

Diabetes/HTN

159
Q

Sixth nerve palsy clinical features

A

Diplopia - worse on horizontal gaze in direction of lesion

Blurred vision

Dizziness

Eye pain

Failed eye abduction - ipsilateral to the lesion

Strabismus - abnormal eye alignment

160
Q

Sixth nerve palsy ix

A

Clinical diagnosis

MRI/CT

ESR/CRP

161
Q

Sixth nerve palsy mx

A

Treatment directed towards underlying cause

Persistent symptoms → patching, use of prisms, strabismus, botox injections (referral to ophthalmology)

Y4 special senses, neurology & dermatology (7 decks)

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