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Phase 2 Med > Neurology > Flashcards

Neurology Flashcards

1
Q

Stroke (ischaemic, haemorrhage) definition

A

Ischaemic stroke = vascular occlusion or stenosis cuts off blood supply to the brain
- most common type of stroke (87%)

Haemorrhagic stroke = vascular rupture, resulting in intraparenchymal and/or subarachnoid haemorrhage - bleeding in brain causes stroke
- 13% of strokes

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2
Q

Stroke aetiology

A

Risk factors both

  • age >55
  • family history
  • HTN, T2DM
  • smoking

Ischaemic

  • Afib
  • history of: TIA, stroke
  • sickle cell disease

Haemorrhagic

  • male
  • asian/black
  • alcohol
  • anticoagulant use
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3
Q

Stroke pathophysiology

A

Other types = subarachnoid haemorrhage and cavernous sinus thrombosis

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4
Q

Stroke clinical manifestations

A

Ischaemic - key

  • vision loss
  • unilateral muscle weakness (often face, arm, leg)
  • impaired language function (aphasia)
  • impaired coordination (ataxia)

Ischaemic - other

  • sensory loss
  • headache
  • diplopia
  • dysarthria
  • gaze paresis
  • arrhythmia

Haemorhhagic

  • visual disturbance (homonymous hemianopia - visual field loss on the left or right side of the vertical midline on the same side of both eyes may be due to haemorrhage in visual pathways, diplopia may result from brain stem haemorrhage)
  • photophobia
  • unilateral muscle weakness/paralysis (often face, arm, leg)
  • dysarthria/dysphasia
  • ataxia
  • sensory loss
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5
Q

Stroke uncommon clinical manifestations

A

Both

  • vertigo
  • nausea/vomiting
  • coma

Ichaemic
- neck/facial pain

Haemorrhagic
- gaze paresis

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6
Q

Stroke 1st line investigations

A

Both
- non-contrast CT head
- serum glucose - hyperglycemia associated with worse prognosis, hypo
= stroke mimc
- serum electrolytes - exclude electrolyte disturbance
- serum urea and creatinine - exclude renal failure
- FBC - exclude thrombocytopenia
- ECG - may indicate MI

Ischamic

  • cardiac enzymes - exclude MI
  • PT and PTT - exclude coagulopathy

Haemorrhagic

  • liver func
  • clotting screen - exclude coagulopathy
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7
Q

Stroke general investigations

A

Both: serum toxicity screen - exclude alcohol/drug causes

Ischaemic

  • CT/MRI - show areas at risk of subsequent infarction
  • US - shows carotid stenosis
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8
Q

Stroke management

A

INITIAL - suspected ischaemic/haemorrhagic stroke

  • first line stabilize and refer to hyperacute/acute stroke unit
  • consider endotracheal intubation
  • give supplementation oxygen only if oxygen saturation drops below 93%

ACUTE - confirmed ischaemic stroke

  • 1st line - monitor: consciousness (Glasgow coma scale), blood glucose, BP, oxygen saturation, hydration, temperature (antipyretic high temp), cardiac rhythm and rate, intracranial pressure
  • IV alteplase
  • mechanical thrombectomy and antiplatelet drug (aspirin)
  • venous thromboembolism prophylaxis and high intensity statin (atorvastatin)

ACUTE - confirmed haemorrhagic stroke

  • 1st line - monitor (as above) and immediate referral to neurosurgery assessment
  • rapid BP control
  • reversal of anticoagulation
  • warfarin/vit K antagonist reversal (prothrombin complex concentrate, phytomenadione)
  • dibigatran reversal (idarucizumab)
  • factor Xa reversal (prothrombin complex concentrate)
  • venous thromboembolism prophylaxis
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9
Q

Transient ischaemic attack (TIA) definition

A

Focal, sudden onset, neurological deficit lasing <24 hours, with complete clinical recovery
15% of first strokes are preceded by TIA

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10
Q

Transient ischaemic attack epidemiology

A

M > F
Black ethnicity is at greater risk due to their hypertension and atherosclerosis predisposition
20, 000 people have a TIA

Risk factors

  • age
  • hypertension
  • smoking
  • diabetes
  • heart disease - valvular, ischaemic or AF
  • past TIA
  • peripheral arterial disease
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11
Q

Transient ischaemic attack aetiology

A

Inadequate cerebral or ocular blood supply due to

  • reduced blood flow
  • ischaemia
  • embolism associated with disease of: blood vessels, heart or blood

Reduced blood flow can be caused by

  • atherothromboembolism from the carotid artery
  • small vessel occlusion
  • cardioembolism resulting in microemboli from
  • mural thrombus post-MI or in AF
  • valve disease
  • prosthetic valve
  • hyperviscocity eg polycythaemia, sickles cell anaemia, extremely raised white cell count, myeloma
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12
Q

Transient ischaemic attack pathophysiology

A

Common cause is from cerebral ischaemia - lack of O2 and nutrients to the brain - cerebral dysfunction
- ischaemia is short lived, with symptoms only lasting a maximum if 5-15 mins after onset and then resolves before irreversible cell death occurs

Gradual progression of symptoms suggests a different pathology eg demyelination, tumour or migraine

90% of TIA’s affect the anterior circulation (carotid artery)
10% affect posterior circulation (vertebrobasilar artery)

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13
Q

Transient ischaemic attack clinical manifestations

A

Sudden loss of function with complete recovery
Stroke symptoms (focal neurological deficit)
- slurred speech
- facial droop

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14
Q

Transient ischaemic attack other diagnostic features

A

Associated with both anterior and posterior circulation TIAs
- unilateral weakness/paralysis

Associated with anterior circulation TIAs

  • dysphasia
  • amaurosis fugax

Aossictaed with anterior circulation TIAs

  • ataxia, vertigo, loss of balance
  • homonymous hemianopia
  • diplopia
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15
Q

Transient ischaemic attack investigations

A

First line:
Blood glucose - exclude hypoglycaemia
FBC/platelet count = normal
PT/PTT/INR - exclude coagulopathy
Fasting lipid profile - normal or hyperlipidemia
Serum electrolytes - exclude electrolyte disorders
ECG - evaluate atrial fibrillation and other arrhythmias (rule out MI)
CT angiography - look for stenosis

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16
Q

Transient ischaemic attack differential diagnosis

A

Impossible to differentiate from a stroke until there is a full recovery
Hypoglycaemia
Labyrinthine disorders - labyrinthitis/vestibular neuronitis, BPPV, Meniere’s disease
Migrainous aura
- typical - visual symptoms, sensory symptoms, dysphagia
- atypical - motor weakness “hemiplegic migraine”

Mass lesions

  • sundural hematoma
  • cerebral abscess
  • tumours

Postictal weakness (also known as Todd’s paralysis)

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17
Q

Transient ischaemic attack management

A 
INITIAL - for suspected transient ischaemic attack 
1st line 
- antiplatelet therapy 
Primary: aspirin 
Secondary: clopidogrel 
Referral 
ACUTE - confirmed TIA 
1st line 
- Antiplatelet therapy 
Primary: clopidogrel 
Secondary: aspirin 
High intensity statin 
- atorvastain 
- simvastatin 
Anticoagulant 
- LMW heparin 
- direct thrombin inhibitor 
- factor Xa inhibitor
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18
Q

Subarachnoid, subdural, extradural haemorrhage definition

A

EDH - bleeding external to dura
SDH - bleeding beneath the dural membrane
SAH - bleeding within the subarachnoid space

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19
Q

Subarachnoid, subdural, extradural haemorrhage epidemiology

A

EDH - adolescents/young adults
- 10% severe head injuries -> EDH

SDH

  • elderly
  • blood thinning medication
  • haemophilia
  • epilepsy
  • alcoholics (chronic alcohol consumption can gradually cause brain to shrink and make blood vessels more vulnerable to damage

SAH - uncommon

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20
Q

Subarachnoid, subdural, extradural haemorrhage risk factors

A

SAH

  • smoking
  • high blood pressure
  • excessive alcohol consumption
  • a family history of the condition
  • some rarer conditions, such as autosomal dominant polycystic kidney disease (ADPKD)
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21
Q

Subarachnoid, subdural, extradural haemorrhage aetiology

A

EDH

  • head strike (sport/motor vehicle accident)
  • fractured temporal or parietal damaging the middle meningeal artery or vein

SDH
- usually trauma causes tearing of subdural cortical bridging veins = blood between dura matter

SAH

  • after trauma where cortical surface vessels are damaged
  • non-traumatic follows the rupture of a cerebral (Terry) aneurysm = blood in circle of willis cisterns and fissures
  • less common - brain tumour; encephalitis; vasculitis
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22
Q

Subarachnoid, subdural, extradural haemorrhage pathophysiology

A

SDH
Bleeding into the subdural space caused by damage to cranial vessels/brain.
As blood starts to build up, it can place pressure on the brain (intracranial hypertension) -> brain damage

SAH
A brain aneurysm is a bulge in a blood vessel, caused by weakness in the blood vessel wall, usually at a point where the vessel branches off. As blood passes through the weakened vessel, the pressure causes a small area to bulge outwards like a balloon and rupture

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23
Q

Subarachnoid, subdural, extradural haemorrhage clinical manifestations

A

EDH

  • initial loss of consciousness -> lucid interval -> second loss of consciousness
  • hemiparesis
  • nausea/vomiting
  • unequa pupils
  • bradycardia

SDH

  • level of consciousness gradually decreases
  • gradual increase of headache and confusion/slurred speech
  • confusion
  • double vision
  • seizures

SAH

  • extremely painful headache
  • thunderclap headache, maximum severity within seconds, worse ever, potential focal symptoms/coma as a result of aneurysms
  • sight problems
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24
Q

Subarachnoid, subdural, extradural haemorrhage management

A

EDH

  • expident evacuation via a craniotomy
  • ABC/2 (haemorrhage volume measurement method)
  • give oxygen
  • a full trauma assessment must be made
  • intravenous (IV) fluids may be required to maintains the circulation and preserve cerebral perfusion
  • if IC pressure is raised -> osmotic diuretics (IV mannitol)
  • Burr holes may be required to evacuate a hematoma

SDH

  • conservative (monitor with serial CT)
  • surgical - craniotomy (main treatment after severe head injury); burr holes (main treatment for hematomas)
SAH 
- nimodipine 
- analgesioa 
anticonvulsant (phenytoin) 
- antiemetic (promethazine) 
- surgery - neurosurgical clippings, endovascular coiling
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25
Q

Subarachnoid, subdural, extradural haemorrhage complications

A

SAH

  • rebleeding
  • delayed cerebral ischaemia
  • coma
  • hydrocephalus
  • epilepsy
  • cognitive dysfunction
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26
Q

Epilepsy definition

A

A recurrent tendency to spontaneous episodes of abnormal electrical activity within the brain which manifest as seizures

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27
Q

Epilepsy aetiology

A

Electrical signals become scrambled and there are sometimes sudden bursts of electrical activity causing seizures.
Very often idiopathic with no clear cause found
Associated with
- underlying structural lesions (trauma, neoplasms, malformations, stroke)
- metabolic conditions (alcohol, electrolyte disorders)
- infections
- rare genetic diseases (eg ion channel mutations)

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28
Q

Epilepsy pathophysiology

A

Classification:
Partial seizures:
- features attributable to a localised part of one hemisphere
- simple partial seizures, consciousness is unimpaired
- complex partial seizures, consciousness is impaired

Generalised seizures:

  • originating bilaterally distributed networks -> simultaneous onset of widespread electrical discharge. No localising features referable to a single hemisphere
  • motor seizures are bilateral
  • more commonly seen in children
  • consciousness is always impaired
  • absence seizures = brief (<10s) pauses eg stopping talking in mid-sentence and then carrying on where left off
  • tonic-clonic seizures = sudden loss of consciousness with stiffening (tonic) of limes and then jerking (clonic)
  • myoclonic jerks = sudden violent movement of the limbs
  • atonic (akinetic) seizures: sudden loss of muscle tone causing a fall, no LOC
  • tonic: sudden stiffening of the body, no jerking
  • infantile spasms: commonly associated with TB

Focal seizures: originating in networks linked to 1 hemisphere and often seen with underlying structural disease

  • subclasses include:
  • without conscious impairment: no post-ictal syndrome
  • with impairment of consciousness: most commonly arise from temporal lobe; post-ictal confusion
  • evolving to bilateral, convulsive seizure
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29
Q

Epilepsy clinical manifestations

A

ICTAL: seizures can present in a number of ways

PREICTAL: preceding prodrome (an early sign or symptom) lasting hours or days in which there may be a change in mood or behaviour
- aura: maybe a strange feeling in the gut or flashing lights (implies a focal seizure, often from the temporal lobe

POSTICTAL

  • headache
  • confusion
  • myalgia (pain in a muscle or group of muscles)

Focal lobe specific postictal symptoms include:

  • temporal lobe: emotional disturbance, dysphagia, hallucinations, bizarre associations
  • frontal lobe: motor features such as pedaling movements of the legs. Motor arrest, dysphagia or speech arrest; Postictal Todd’s Palsy: limb paralysis in a seizure for several hours
  • parietal lobe: sensory disturbances - tingling, numbness, pain. Motor symptoms
  • occipital lobe: visual phenomena such as spots, lines, flashes
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30
Q

Epilepsy differential diagnosis

A
  • migraine
  • TIA
  • cardiogenic syncope
  • parasomnia
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31
Q

Epilepsy management

A

Pharmacology: anti-epileptic drugs (main treatment)
Do not give sodium valproate to pregnant women. Women on childbearing age should be on contraception (not just condoms)

Psychological therapies:

  • relaxation
  • CBT

Surgical intervention

  • neurosurgical resection
  • vagus nerve stimulation is a palliative treatment option for refractory epilepsy

Lifestyle: ketogenic diet can help control seizures

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32
Q

Parkinsons definition

A

Chronic progressive neurological disorder characterised by motor symptoms of resting temor rigidity, bradykinesia and postural instability

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33
Q

Parkinsons key clinical manifestations

A
  • presence of risk factors (age, family PD, mutations in GBA gene)
  • bradykinesia (progressive slowness of movement)
  • resting trmor
  • rigidity
  • postural instability
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34
Q

Parkinsons other clinical manifestations

A
  • masked facies (loss of spontaneous face movement)
  • hypophonia (reduced voice vol)
  • hypokinetic dysarthria
  • micrographic (decreased amplitude of handwriting)
  • stooped posture
  • shuffling gait
  • fatigue
  • constipation
  • depression
  • anxiety
  • dementia
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35
Q

Parkinsons 1st line investigations

A

Dopaminergic agent trial

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36
Q

Parkinsons 2nd line investigations

A
  • Brain MRI
  • Functional neuroimaging (dopamine transporter imaging) - look for decreased basal ganglia presynaptic dopamine uptake
  • olfactory testing looks for hyposmia or anosmia
  • genetic testing
  • neuropsychometirc testing
  • serum ceruloplasmin excludes Wilson’s disease
  • 24 urine copper excludes Wilson’s disease
  • postmortem brain pathology
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37
Q

Parkinsons management

A

Mild Parkinson’s:
1st line - MAO-B inhibitor, dopaminergic agent, amantadine or trihexyphenidyl
Primary options:
- rasagline (MAOi)
- pramipexole (dopamine agonist)
- ropinirole (dopamine agonist)
- carbidopa/levodopa (converts to dopamine)
- rotigotine transdermal (dopamine agonist)
Secondary:
- selegiline (MAOi)
- trihexyphenidyl (anticholinergic)
- amantadine (increase amount of dopamine)
- also physical activity
- additional carbidopa or domperidone (dopamine antagonist) for nausea

Moderate Parkinson’s:
First line - MAO-B inhibitor, dopaminergic agen, amantadine or trihexyphenidyl
- pharmacotherapy/deep brain stimulation
- propanolol
- primidone
- reduce dopaminergic medications

Advanced Parkinson’s:
First line - MAO-B inhibitor, dopaminergic agent, amantadine or trihexyphenidyl
- deep brain stimulation and intrajejunal infusion of levodopa

General

  • physical therapy
  • occupational therapy
  • speech and language therapy
  • diet advice
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38
Q

Headaches - migraine, tension cluster, drug overdose epidemiology

A

Early-mid life

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39
Q

Headaches risk factors

A

Family history

  • high caffeine intake
  • female sex/obesity
  • stressful life events/sleep disorders

Mental tension

  • stress
  • missing meals
  • fatigue
  • female sex

Male sex

  • family history
  • head injury
  • smoking
  • heaving drinking
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40
Q

Headaches pathophysiology

A

Classifications

  1. Primary (have no diagnostic test, diagnose based on symptoms)
    - migraine - w/wihtout aura
    - tension - mild/moderate ‘squeezing’, not aggregated by physical activity
    - cluster
  2. Secondary (consider if older, immunosuppressed, previous cancers)
    - meningitis
    - subarachnoid haemorrhage
    - giant cell arthritis
    - idiopathic intracranial hypertension - can affect vision
    - medication overused headache
  3. Other
    - trigeminal neuralgia (facial pain)
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41
Q

Headaches clinical manifestations (migraine)

A

Episodic/20% with aura or chronic
Moderate to sever pain, lasting 4-72 hours
Aggravated by routine physical injury
Unilateral, nausea/vomiting, photophobia/phonophobia

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42
Q

Headaches clinical manifestations (tension)

A

Bilateral, pressing, tightening, mild.moderate intensity,
Stress = common trigger, not aggravated by physical activity
No nausea/vomiting
Potential photophobia/phonophobia

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43
Q

Headaches clinical manifestations (cluster)

A

Unilateral, orbital, supraorbital and temporal
Extremely painful
Attacks same time for several weeks
Accompanied with ipsilateral cranial autonomic features
Sense of relentlessness or agitation
Generally shorter episodes than migraine

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44
Q

Headaches clinical manifestations (medicine overuse)

A

Present on >15 days a month
Common medicines
- ergotamine, triptans, opioids, analgesics.
Headahce develops/markedly worsens during drug use.
Can lead to chronic daily headache
- (if headache happens over 50% of the time)

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45
Q

Headaches clinical manifestations (trigeminal neuralgia)

A

Short paroxysmal attacks, electric shock like, precipitated by innocuous stimuli to affected side of face

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46
Q

Headaches clinical manifestations (secondary)

A

Postural headaches are suggestive of secondary
Neck stiffness - possibly meningitis
Sudden onset thunderclap (suggests vascular)

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47
Q

Headaches clinical manifestations (red flags - brain tumour)

A 
New headache with Hx of cancer 
Cluster headache 
Seizure 
Significantly altered consciousness, memory, confusion, coordination 
Papilloedema
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48
Q

Headaches investigations

A

Primary - no diagnostic tests - classify based on symptoms
May do other tests to rule out other causes (not diagnostic), all these tests should be normal if patient has a migraine/tension/cluster
- ESR - rule out temporal arteritis
- Lumbar puncture - rule out: SAH, meningitis
- CFR culture - rule out systemic/NS infection
- MRI brain - rule out ischaemic lesions
- CT of head - rule out lesions, SAH
- pituitary func test - rule out pituitary adenoma
- ECG - rule out conduction abnormalities

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49
Q

Headaches differential diagnosis

A

Tension/cluster headaches, MOH, SAH, giant cell arteritis, CVT
Chronic migraine, sphenoid sinusitis
Migraine, paroxysmal hemicrania, SUNCT

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50
Q

Headaches management

A

MIGRAINE: lifestyle modification and trigger management
- lying in a dark room
Pharmacological treatments:
- offer topiramate or propanolol (for avoiding attacks, taken regularly)
- botulinum toxin A injections can work in chronic cases
- NSAIDS (aspirin, ibuprofen, naproxen)
- pain killers (paracetamol, ketorolac)
- triptan (migraine specific pain killer) (sumatriptan, almotriptan, eletriptan); often effective to combine with another painkiller)
- anti-sickness medication (metoclopramide, prochlorperazine, promethazine, compazine, thorazine, reglan)
- antihistamine (in acute M) (diphenhydramine, promethazine)
Hydration
High flow O2
Surgical treatment
- decompression (removes tissue putting pressure on peripheral sensory nerves)
- neurectomy (cuts nerve in head contributing to migraine symptoms)
- acupuncture
- TMS = brain stimulation

TENSION HEADACHES 
Non-pharmacological treatment 
- relaxation techniques: yoga/massage 
- exercise 
- EMG biofeedback 
- CBT 
- acupuncture 
- physiotherapy 
Pharmacological treatment: 
- Acute: simple analgesics (aspirin, paracetamol, ibuprofen, naproxen) 
- chronic: - antidepressants (amitriptyline, doxepin, venlafaxine); muscle relaxants (tizanidine) 
CLUSTER HEADACHES 
Pharmacological 
- 1st line: sumatriptan, oxygen 
- zolmitriptan 
- anaesthetic (lidocaine) 
- CCB (verapamil) 
- AEDs (topiramate) 
Non-pharmalogical 
- greater occipital nerve block 
- surgery (deep brain stimulation) 
MOH 
Stop taking medication
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51
Q

Multiple sclerosis definition

A

Inflammatory autoimmune demyelinating central nervous system condition characterised by the presence of episodic neurological dysfunction in at least two areas of the central nervous system

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52
Q

Multiple sclerosis epidemiology

A

Caucasian
Women (F:M, 3:1)
20-40 years

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53
Q

Multiple sclerosis pathophysiology

A

Oligodendrocytes affected not Schwann cells
Classification
1. macrophage mediated demyelination
2. antibody mediated demyelination
3. distal oligodendrogliopathy and apoptosis
4. primary oligodendroglial degeneration

Type of MS progression

  • relapsing/remitting (attacks are in discrete time sets, go back to normal after each attack or disability will progressively get worse between attacks)
  • primary progressive (patient gets progressively worse, or at accelerated/decelerated rate)
  • secondary progressive (following an initial attack the disease will get progressively worse)
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54
Q

Multiple sclerosis clinical manifestations

A

Typical:

  • optic neuritis (painful progressive visual loss)
  • spasticity and other pyramidal signs
  • sensory symptoms and signs
  • Ihermitte’s signs (electric shock down back of spine)
  • Nystagmus (involuntary movements)
  • double vision and vertigo (spinning / dizziness)
  • bladder and sexual dysfunction

Atypical:

  • aphasia (can’t comprehend language)
  • hemianopia
  • extrapyramidal movement disturbances
  • severe muscle wasting
  • muscle fasciculation (all grey matter issues or peripheral nerve issues)

Patients more commonly present with weakness, paraesthesia, visual loss, as opposed to incontinence.

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55
Q

Multiple sclerosis 1st line investigations

A

MRI-brain (sagittal FLAIR)
MRI-spine (demyelinating cervical spinal cord lesions are common)
FBC - excludes alternative diagnosis (should be normal)
Comprehensive metabolic panel - excludes alternatve dianosis (should be normal)
Thyroid stimulating hormone - excludes alternative diagnosis (should be normal)
Vit B12 - excludes alternative diagnosis (should be normal)
Anti-neuromyelitis optica antibody - present in neuromyelitis optica
Cerebrospinal fluid evaluation - elevated CSF IgGs in 80% of MS

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56
Q

Multiple sclerosis differential diagnosis

A

Autoimmune disorders

  • systemic lupus erythamtous
  • primary sjogrens syndrome
  • Bhcet’s disease
  • polyarteritis nodosa
  • acute disseminated encephalomyelitis
Infectious disease 
- lyme 
- syphilis 
- AIDS 
Adrenomyeloneuropathy 
Mitochondrial encephalopathy 
Arnold-chirari malformation 
Olivopontocerebellar atrophy 
Cardiac emboli event
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57
Q

Multiple sclerosis management

A

Acute relapsing MS:

  • immunimodulatory therapy for acute relapse (5 day course of corticosteroid prednisolone - symptomatic modifying; anti-inflammatory cytokine Betaferon - disease modifying)
  • oral/IV methylprednisolone
  • plasma exchange

Relapse-remitting MS:
- immunomodulatory (interferon B)

Symptomatic treatment:

  • medications for fatigue (amantadine, modafinil, armodafinil)
  • visual problems (steroids - gabapentin)
  • muscle spasms (physiotherapy
  • mobility problems (exercise program, mobility aids)
  • neuropathic pain (gabapentin, crabamezapine)
  • MSK pain (exercise techniques, painkillers, TENS machine)
  • emotional problems (antidepressant, benzodiazepines, CBT)
  • sexual problems (viagra)
  • bladder problems (catheter)
  • bowel problems (changing diet, laxative)
  • temor (propanolol)

Secondary progressive:

  • 1st line - siponimod or methylprednisolone
  • cladribine

Progressive:
- ocrelizumab

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58
Q

Motor neurone disease definition

A

A cluster of neurodegenerative disease

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59
Q

Motor neurone disease epidemiology

A

Most cases are sporadic. More common in middle aged men

60
Q

Motor neurone disease classification

A

Amylotrophic later sclerosis (80%):

  • loss of neurons in the motor cortex and the anterior horn
  • combined UMN and LMN signs

Progressive bulbar/pseudobulbar palsy (10-20%)

  • only affects cranial nerves IX-XII
  • worst prognosis

Progressive muscular atrophy (<10%)

  • anterior horn cell lesion
  • best prognosis
  • LMN signs only and distal muscle groups affected first

Primary lateral sclerosis (rare)
- progressive tetraparesis

With all there is no sensory loss and it never affects eye movements

61
Q

Motor neurone disease pathophysiology

A

Characterised by selective loss of neurons in motor cortex, cranial nerves nuclei and anterior horn cells

62
Q

Motor neurone disease clinical manifestations

A

UMNL

  • lesion above the anterior horn in the spinal cord or above the nuclei of the cranial nerves
  • ‘everything goes up’
  • increased spasticity +/- clonus (involuntary muscle contractions)
  • increased reflexes
  • extensor plantar response
  • abscent fasciculations ( muscle twitch)

LMNL

  • lesion in anterior horn, motor nerve fibre or neuromuscular junction
  • ‘everything slows down’
  • reduced tone
  • deep tendon reflexes absent or reduced
  • plantar response normal or absent
  • fasciculations may be present
  • muscle wasting usually present

Bulbar palsy - lower motor neuron lesion to CN IX, X, XI, XII

  • dysphagia, chewing difficulties
  • flaccid, fasciculation tongue
  • quiet/nasal/hoarse speech
  • normal/absent jaw jerk reflex

Pseudobulbar palsy - upper motor neuron lesion to CN IX, X, XI, XII

  • dysphagia
  • slow tongue movements
  • small, stiff, spastic tongue
  • slow, indistinct speech
  • increased jaw jerk reflex
Emotional liability - difficulty stopping crying/laughing in inappropriate situations 
Cognitive changes 
Generalised paralysis (bilateral)
63
Q

Motor neurone disease investigations

A

Clinical diagnosis
Electromyography (EGM) shows muscle denervation but not specific
Brain/cord MRI to exclude structural causes
LP to exclude inflammatory causes

64
Q

Motor neurone disease management

A

Incurable so instead symptom management
Occupational therapy
Physio
Riluzole, can slow progression of condition
Medicine to relieve muscle stiffness and help saliva problems

65
Q

Motor neurone disease prognosis

A

Poor, death within 3yrs in 50%

66
Q

Infections - meningitis definition

A

Inflammation of lepto-meninges and underlying subarachnoid CSF

67
Q

Infections - meningitis epidemiology

A

Mainly the young and elderly
3,200 cases of bacterial meningitis occur in the UK ps,
3,000 cases of viral meningitis

68
Q

Infections - meningitis aetiology

A

Viral - around 80% of meningitis cases

  • enterovirus (echo virus, coxsackie virus)
  • herpes simplex virus
  • Varicella-zoster virus
  • EBV (epstien-barr)
  • CMV (cytomegalovirus)

Bacterial

  • Neisseria meningitidis (meningococcus) - gram-ve diplococci
  • Streptococcus pneumpniae - gram+ve diplococci
  • Listeria monocytogenes
  • Hamophilius influenzae
  • Escherichia coli and Group B Streptococcus - in neonates

Intrathecal drug
Microorganism reach meninges by (direct from ears, nasopharynx, cranial injury, bloodstream)

Risk factors

  • CSF shunts
  • immunocompromised (HIV, cancer)
  • Bacterial endocarditis, T2DM, alcohol and cirrhosis, IV druguse, renal insufficiency, adrenal insufficiency, malignancy, hyperparathyroidism, thalassaemia, CF
  • splenectomy and sickle cell disease
  • age (<5yrs, >60yrs)
69
Q

Infections - meningitis pathophysiology

A

Viral meningitis = more common and benign than bacterial meningitis

Meningococcal disease (illnesses caused by N.meningitidis)

  • presents as bacterial meningitis (15%)
  • septicaemia (25%)
  • combination of 2 presentations (60%)
70
Q

Infections - meningitis clinical manifestations

A

Early:

  • fever, headache
  • leg pain
  • cold hands/feet

Later:
- stiff neck, back rigidity, bulging fontanelle
- photophobia
- altered mental state, unconsciousness, coma
- Kernig’s sign
- Brudzinski’s sign (forced flexion of the neck elicits a reflex flexion of the hips)
- paresis
- raised ICP - low GCS, seizure, focal deficits
- septic shock - (suggestive of meningococcal)
- vomiting
- papilledema
- progressive dorwsiness, lateralizing signs
Viral m. features may be milder and complications less frequent

Meningisn:

  • neck stiffness
  • photophobia
  • non-blanching petechial rash/purpura (menigococcal only)
  • Kernig’s sign (thigh is flexed at the hip and knee, subsequent extension in knee is painful
71
Q

Infections - meningitis investigations

A

1st line: bloods - culture, FBC, CRP, glucose, lactate, VBG, nose and throat swabs
2nd line: lumbar puncture - contraindicated if raised ICP, shock, coagulation abnormalities

72
Q

Infections - meningitis management

A

IV fluids - prevent dehydration
Oxygen if breathing difficulties
Steroids - can reduce swelling in the brain

Prevention by:

  • meningococcal vaccine (same for meningococcal disease)
  • Hib vaccine
  • pneumococcal vaccine
73
Q

Infections - meningitis complications

A

Bacterial:
Spetic shock, disseminated intravascular coagulation, coma with loss of protective airway reflexes, cerebral oedema and raised intracranial pressure, spetic arthritis, pericardial effusion and haemolytic anaemia (H, influenzae)
Subdural effusions: reported in 40% of children aged 1-18 months with bacterial meningitis. Risk factors include young age, rapid onset of illness, low peripheral white cell count and high CSF protein.
Syndrome of inappropriate antidiuretic hormone secretion (SIADH)
Seiures
Decreased hearing, or deafness; other cranial nerve dysfunction, multiple seizures, focal paralysis, subdural effusions, hydrocephalus, intellectual deficits, ataxia, blindness, Wtarehouse-Friderchsen syndrome and peripheral gangrene.
Venous sinus thrombosis, severe cerebral oedema, cerebral abscess

Viral: rarely occur

74
Q

Infections - meningitis prognosis

A

Meningitis kills more UK children under the age of 5 than any other infectious disease

75
Q

Encephalitis defintion

A

Inflammation of the brain

76
Q

Encephalitis epidemiology

A

Age (<1, >65)
Immunodeficient
HSV (herpes simple virus)

77
Q

Encephalitis aetiology

A

An infection spreads to the brain - usually viral

Herpes viruses:

  • herpes simple virus (most common cause)
    1. cold sores/fever
    2. genital herpes
  • Epstein barr
  • Varicella zoster (chickenpox/shingles)

Enterovirus:

  • polio
  • coxsackievirus (flu, eye inflammation, ab pain)

Childhood infections:
- measles, mumps, rubella

Animal spread:
- tick-born, Japanese encephalitis, rabies, West Nile virus)

USUALLY viral but can be bacterial, fungal and parasitic:

  • bacteria: mycoplasma, meningococcal, pneumococcal listeria.
  • fungi: histoplasma, cryptococcus, candida
  • parasites: malaria, toxoplasma
78
Q

Encephalitis risk factors

A
  • viral infections
  • organ transplant
  • animal/insect bites
  • location
  • season
79
Q

Encephalitis pathophysiology

A

Infection and non-infectious causes

Infectious (primary):

  • agent directly infects the brain
  • viral/bacterial/fungal.parasitic

Non-infectious (secondary)

  • faulty immune system reaction to infection elsewhere in body - immune system accidentally also attacks health cells in the brain
  • autoimmunity
80
Q

Encephalitis clinical manifestations

A
  • headache
  • seizures
  • cough
  • GI infection
  • focal neurological signs
  • fever
  • rash
  • altered mental state
  • meningismus
  • parotitis
  • lymphadenopathy
  • optic neurtisi
  • acute flaccid paralsis
  • movement disorder
  • bisphasic illness
  • myocarditis/pericarditis
  • jaundice
  • arthirits (lyme disease)
  • retinitis (Wets Nile virus)
  • Parkinsonism (arbovirus)
81
Q

Encephalitis 1st line investigations

A
  • blood cultures (confirms Bacterial E. and most arboviral infections)
  • FBC (elevated WCC)
  • peripheral blood smear (detects P. falciparum/ehrlichia)
  • serum electrolytes (hyponatraemia)
  • liver function tests = elevated
  • throat swab - detect viruses
  • nasopharyngeal aspirate (detects resp viruses); go on to do PCR to confirm adenovirus/influenza
  • sputum culture (detect mycoplasma, TB and fungal infections
  • chest x-ray (detect non infectious/infectious causes)

Neuroimaging:

  • MRI - will differ depending on aetiology
  • CT scan
  • CSF (lumbar picture) - analysis; culture; serology; PCR
  • ECG
82
Q

Encephalitis 2nd line investigations

A
  • urine culture - detects polio, varicella zoster, mumps, measles
  • stool enteroviral culture
  • IgG/IgM antibodies in blood - may identify aetiology
  • PCR
  • HIV serology /RNA test
  • CSF biomarkers
  • whole body CT/PET - identify cancers
83
Q

Encephalitis management

A

Treat underlying cuase:

  • antiviral medication; acyclovir, ganciclovir, foscarnet
  • anti-inflammatory drugs; corticosteroid - if E. is caused by a problem with the immune system
  • immunoglobulin therapy
  • plasmapheresis
  • surgery to remove tumur
  • antibiotics or antifungals

Encephalitis puts strain on the body and relieves symptoms

  • fluids to prevent dehydration
  • painkillers to reduce discomfort or high temp
  • medicine to control seizure or fits
  • medicine to help the person relax
  • oxygen to support lungs
  • medicine - prevent a build up of pressure

Acyclovir - for viral E.

84
Q

Encephalitis complications

A
  • seizures
  • hydrocephalus
  • neurological sequelae
85
Q

Herpes zoster definition

A

Shingles also known as herpes zoster is caused by reactivation of varicella-zoster virus (VZV) that was acquired during a primary varicella infection

86
Q

Herpes zoster aetiology

A

Reactivation of latent VZV from dorsal root or cranial nerve ganglia present since primary infection. Herpes zoster and varicella (chicken pox) are both caused by VZV but varicella usually follows he initial infection and causes a generalised rash whereas HZ occurs after activation of a previous infection and tends to be localised to a specific nerve distribution.

87
Q

Herpes zoster pathophysiology

A

Immunocompromisation such as HIV, malignancy, chemo and chronic use of corticosteroids.
Infection spreads from a ganglion to the corresponding cutaneous neural tissue
Most common dermatomes are T1 to L2

88
Q

Herpes zoster clinical manifestations

A

Characterised by dermatomal pain and papular rash. Pain typically precedes the rash by several days and can persist for months after the rash resolves. Rash usually presents in a single dermatome and typically resolves within 4-5 weeks

Key:

  • localised burning, stinging, itching or tingling in a dermatome
  • pruritus may resent in affected dermatome
  • erythematous maculopapular rash
  • corneal ulceration (if trigeminal nerve is affected)
89
Q

Herpes zoster investigations

A

Usuaully clinical diagnosis

May need PCR

90
Q

Herpes zoster management

A

Antiviral therapy: famciclovir if immunicompetent aciclovir if immunocompromised

91
Q

Herpes zoster complications

A

HZ ophthalmicus
Superinfection of skin lesions
Postherpetic pain is common

92
Q

Dementia - AD, vascular, lewy body, frontotemporal definition

A

Group of chronic, progressive neurogenerative disorders

93
Q

Dementia aetiology

A

Alzheimer’s (50%): atrophy, neurofibrillary tangles, amyloid plaques, neuronal loss

Vascular (25%): brain damage due to cerebrovascular disease

Lewy Body (15%): deposition of abnormal protein in brain stem and neocortex

Frontotemporal (5%): atrophy of frontal and temporal lobes. Most common dementia in user 65s

94
Q

Dementia risk factors

A

AD: old age, family history, Down’s
Vascular: old age, obesity, HTN, smoking
Frontotemporal: genetic mutations

95
Q

Dementia pathophysiology

A

AD: extracellular deposition of beta-amyloid plaques, tau intracellular neurofibrillary tangles, damaged synapses and atrophy are the pathological hallmarks

Lewy body: deposition of levy body inclusions, neurofibrillary tangles and a deficit of ACh and dopamine (causing Parkinsonism)

96
Q

Dementia clinical manifestations

A

Alzheimer’s:

  • progressive short term memory loss
  • disorintation
  • nominal dysphasia
  • getting lost
  • decline in ADLs (activities of daily activity)

Vascular: stepwise progression (stable symptoms followed by sudden increase in severity), stroke history, poor attention, abnormal reflex responses (jaw-jerk,glabella tap)

Lewy body: fluctuating conginition, recurrent visual hallucinations, REM sleep behaviour disorder, parkinsonism

Frontotemporal: park incidence = 50-60s behavioural/personality change, loss of language fluency/comprehension, abandonment of work and activities

97
Q

Dementia management

A

Alzheimer’s: supportive

Vascular: treat atherosclerosis, lifestyle modifications, antiplatelets, statins, antihypertensive

Lewy Body:

  • behavioural disturbances: benzodiazepines
  • psychotic symptoms: cholinesterase inhibitors
  • REM sleep problems: SSRI
  • motor symptoms: clonazepam, melatonin, carbidopa

Frontotemporal

  • no cure
  • SSRIs for behavioural symptoms
  • Levodopa/carbidopa if parkinson’s symptoms present
98
Q

Primary and secondary tumours classification

A

Classification by cell of origin

Glial cells: astrocytoma, oligodendrocytoma, ependymoma, glioblastoma

Primitive neuroectodermal cells: medulloblastoma, neuroblastoma

Arachnoidal cell: meningioma

Nerve sheath cell: schwannoma, neurofibroma

Lymphoreticular cells: lymphoma (primary CNS lymphoma)

Histological classification

  1. Neuroepithelial (neuroepithelial cells are stem cells that differentiate into neurons and glial cells)
    - astorcytic - glioblastoma, pilocytic astrocytoma
    - oligodendroglioma
  2. Meningeal - meningioma (mostly benign)
  3. Metastatic - commonly in lung, breast, colorectal, testicula, renal cell, malignant melanoma
  4. Others - pituitary oedema, CNS lymphoma, germ cell tumours (rare paediatric, usually malignant), sella region (eg craniopharyngiomas, cystic tumours)
  5. Nerve sheath - schwannoma (can affect cranial nerves eg CN VIII - acoustic neuroma), neurofibroma
99
Q

Primary and secondary tumours epidemiology

A

Gliomas - most common primary brain tumour (glioblastoma are the most common adult brain tumour, astrocytomas are the most common in children), high grade gliomas (grade III and IV) make up 85% of all new cases of all new cases of malignant primary brain tumours

100
Q

Primary and secondary tumours clinical manifestations

A

Cardinal Features
Features of raised ICP:
- headache - worse in morning and lying down, associated with N&V, exacerbated by coughing, sneezing, drowsiness - bear in mind headaches are very common and not much more common than in general population red flags: features of raised ICP (papilloedema and CN VI palsy)
- papilloedema

Progressive focal neurological deficits:

  • hemiparesis
  • hemisensory loss
  • visual field defect
  • dysphasia

Epileptic seizures

Reg flags: new focal symptoms, unilateral, awakes at night

101
Q

Primary and secondary tumours management

A

Dexamethasone - reduce oedema around tumour
Resective craniotomy +/- biopsy
Radio/chemo available but limited

102
Q

Vasculitis definition

A

Conditions where there is inflammation of blood vessels. Most cases are idiopathic. Classified into large, medium, small vessel variable vessel, signal organ and systemic disease-associated

103
Q

Vasculitis presentation

A

Large vessel: HTN, anurysms, dissection, end-organ ischaemia
Medium vessel: ulcers, nodules, lesions, HTN
Small vessel: purpura, ting papules, splinter haemorrhages, urticaria

104
Q

Vasculitis diagnosis

A

Full history
Bloods
Creen for Antinuclear antibodies (ANA)

105
Q

Vasculitis management

A

Corticosteroids - control acute symptoms
Immunosupression - methotrexate, azathioprine
Plasmapheresis

106
Q

Giant cell artiritis (GCA) definition

A

A granulomatous vasculitis of large and medium sized arteries. It primarily affects branches pf the external carotid artery and its branches such as the superficial temporal artery and is the most common form of systemic vasculitis in adults.

107
Q

Giant cell artiritis epidemiology

A

Typically occurs in people >50yrs and is more common in women. Associated with polymyalgia rheumatica

108
Q

Giant cell artiritis aetiology

A

Likely genetic and possibly infective factors

109
Q

Giant cell artiritis pathophysiology

A

Extracranial branches of the carotid artery are preferentially involved although the aorta and its branches may be affected. Affected arteries contain granulomas and may have multinucleate giant cells present although they are not needed for diagnosis of GCA. Inflammation leads to proliferation of myofibroblasts, new vessel formation and marked thickening of the intimal or inner layer. This process leads to narrowing or occlusion of the vessel lumen, ultimately causing tissue ischaemia.
Symptoms derive from ischaemia to organs such as the eye and brain leading to blindness and storke.

110
Q

Giant cell artiritis clinical manifestations

A

Headache - usually temporal or occipital areas
Polymyalgia rheumatica symptoms - aching and stiffness in neck and joints after a period of inactivity and with movement
Extremity claudication
Cranial artery abnormalities - occipital, postauricular or facial arteries may be

Can cause jaw claudication, visual symptoms, tender temporal arteries

111
Q

Giant cell artiritis investigations

A

Bloods: ESR & CRP raised, often have normochromic normocytic anaemia with normal WBC and elevated platelets

Temporal artery USS and Biopsy

112
Q

Giant cell artiritis management

A

1st line: Prednisolone - start immediately if suspected
- may want to start with methylprednisolone pulse therapy
Adjunct: aspirin (lower risk of vision loss and stroke)
Consider osteoporosis prevention (glucocorticoid use): calcium carbonate

113
Q

Giant cell artiritis complications

A 
Large vessel stenosis (especially subclavian and axillary arteries) 
Aortic aneurysm (thoracic are much more likely)
114
Q

Spinal cord compression and cauda equina definition

A

Spinal cord compression: results from processes that compress or displace arterial, venous or cerebrospinal fluid spaces as well as the cord itself

Brown-Sequard syndrome: hemisection of spinal cord usually due to penetrating trauma

Cauda equina syndrome: occurs when the nerves below the end of the spinal cord (cauds equina) is damaged. It is a surgical emergency

115
Q

Spinal cord compression and cauda equina aetiology

A

Spinal cord compression:
Trauma
- usually vertebral fractures or facet joint dislocation
- complete transection of the spinal cord
- hemisection (brown-sequard syndrome) usually caused by a penetrating trauma

Tumours (benign and malignant)

  • bone tumours, primary/metastatic tumours
  • common sites of primary tumours are breats, prostate and lung
  • lymphoma, myeloma
  • neuro tumours eg schwannoma, neurofibroma

Prolapsed intervertebral disc

  • L4/5 and L5/S1 are the most common site for disc prolapse
  • large disc herniation can cause Cauda equina syndrome

Epidural/subdural hematoma
Inflammatory disease, especially RA
Infection

116
Q

Spinal cord compression and cauda equina pathophysiology

A

Spinal cord compression:
Injury to the spinal cord or nerve roots arises from stretching or from pressure. This results in injury to the white matter (myelinated tracts) and grey matter (cell bodies) in the cord with loss of all or some of the sensory modalities (pinprick, joint position sense, vibration, hot/cold, pressure) and motor function

117
Q

Spinal cord compression and cauda equina clinical manifestations

A 
Spinal cord compression 
Red flag signs: 
- loss of bladder or bowel function 
- UMN signs in lower limbs (eg clonus, hyperreflexia) 
- LMN signs in upper limbs (eg atrophy)

Symptoms depend on injury type and sit:

  • paraplegia
  • pain
  • paraesthesia
  • changes to tendon reflexes

Cauda equina syndrome

  • bilateral neurogenic sciatica (pain going down the leg from the lower back, along the course of the sciatic nerve)
  • reduced perineal sensation
  • altered bladder function with painless retention
  • loss of anal tone (bowel dysfunction)
  • loss of sexual function

Brown-Sequard Syndrome

  • ipsilateral hemiplagia with contralateral pain and temperature sensation deficits (due to crossing of fibres in spinothalamic tracts)
  • this is a theoretical injury, it is almost impossible to get a spinal cord injury where you damage the spinal cord exactly in half like this
118
Q

Spinal cord compression and cauda equina investigations

A

Spinal cord compression:

  • spine X-ray is 1st line
  • MRI spine - imaging of choice

Cauda eqina:

  • medical emergency - immediate referral
  • rectal exam - loss of anal tone/sensation
  • MRI is the preferred investigation although often shows no abnormality

Brown-Sequard Syndrome:

  • plain radiographs (X-ray) is 1st line
  • MRI for extent of injury
119
Q

Spinal cord compression and cauda equina management

A

Spinal cord compression:

  • immobilisation essential
  • decompressive/stabilisation surgery
  • dexamethosone until treatment plan confirmed

Cauda equina
- surgical decompression is essential

Brown-Sequard

  • spine immobilisation
  • steroids for swelling
120
Q

Myasthenia gravis definition

A

Autoimmune destruction of Ach (nicotinic) receptors at the neuromuscular junction (NMJ) mediated by ACh receptor antibodies (anti-AChR)

Peak incidence around 30 and 60 years. Twice more common in women

Associated with: SLE, RA, thyroid disease, pernicious anaemia, thymic hyperplasia (wmone>50yrs), thymic atrophy and tumours

121
Q

Myasthenia gravis clinical manifestations

A

Muscle weakness that is worse on exertion and gets better with rest. Ocular muscles are usually involved first (ptosis and diplopia). Often partial or unilateral, improves after sleep and improves with putting an ice pack on the lid.

Fatigable ptosis (eyelid droop) and mysathenia snarl (snarling expression when attempting to smile) may be present.

Progression of weakness is usually top down: extraocular -> bulbar -> face -> limb girdle -> trunk

Weakness is more marked in proximal muscles. No muscle wasting, sensation is unimpaired.

Seizures can occur

122
Q

Myasthenia gravis investigations

A

Anti-AchR antibodies (specific for MG)
Nevre conduction studies (NCS): characteristic decrement in potential
Mediastinal imaging with CT or MRI to look for thymoma
Tensilon test (IV of anticholinesterase) - rarely required

123
Q

Myasthenia gravis management

A

Symptomatic control: anticholinesterase eg pyridostigmine
Relapse treatment:
- immunosuppression with prednisolone (and osteoporosis prophylaxis) - azathioprine etc may be used
- plasmapheresis and IV Ig
- thymectomy if needed (thymoma)

Exacerbating drugs:

  • ciproflaxin, azithromycin
  • propanolol, atenolol
  • verapamil
  • lithium
  • statins
  • chloroquine
  • prednisolone
124
Q

Peripheral neuropathies definition

A

Peripheral neuropathy refers to any disorder of the peripheral nervous system.
Acute or chronic.
Acute neuropathies (such as Guillian-Barre syndrome) eveolve very rapidly.
Chronic neuropathies can be further classified into small fibre and large fibre neuropathies. Neurophysiology helps to divide large fibre into axonal or demyelinating. Chronic demyelinating neuropathies are usually genetic or inflammatory (eg CIDP). These are generally seen by specialist neurologists whereas axonal neuropathies are seen more in primary care and hospital.

Nerve fibres:

  • Aa (large myelinated) - proprioception signals
  • Ab (large myelinated) - light touch, pressure, vibration
  • small myelinated - pain, cold sensation
  • C (small unmyelinated) - pain, warm sensation

Mononeuropathy = problem with one nerve

  • carpal tunnel syndrome (median nerve)
  • ulnar neuropathy (entrapment at the cubital terminal)
  • peroneal neuropathy (entrapment at the finular head)
  • cranial mononeuropathies (III or VIII CN palsy) - idiopathic, immune mediated, ischaemic
Polyneuropathy = problem with many nerves 
Axonal: 
- systemic disease: diabetes mellitus 
- infectious (hep, HIV, lyme) 
- ischaemic (vasculitis) 
- metabolic (Fabry's, porphyria) 
- hereditary (CHarcot-Marie-Tooth) 
- toxins 
Demyelinating 
- Guillain Barre syndrome

Mononeuritis Multiplex (multifocal neuropathy) - two or more nerves in disparate parts of the body

125
Q

Peripheral neuropathies aetiology

A

Diabetes is the most common cause
Can also be due to: dietary deficiencies, medicines, alcohol excess, CKD, injury, infection, connective tissue disorders, inflammatory conditions, some hereditary diseases

Segmental demyelination: from guillain barre syndrome and charcot-marie-tooth disease

126
Q

Peripheral neuropathies pathophysiology

A

Several mechanisms can cause nerve dysfunction

Demyelination: when Schwann cells are damaged the myelin sheath is damaged. This causes marked slowing of conduction, seen for example in Guillain-Barre syndrome.

Axonal degeneration: primary damage is in the axons which dies back from the peripheries

Wallerian degeneration: changes following nerve section (cut). Both axon and distal myelin sheath degenerate over several weeks.

Compression: focal demyelination at the point of compression. This occurs particularly in entrapment neuropathies (eg Carpal Tunnel Syndrome)

Infarction: microinfarction of the vasa nervorum (supplies nerves with blood) occurs in arteritis occurs in diabetes mellitus.

Inflitration: inflammatory cell inflitration due to leprosy, malignant cells or granulomas in sarcoidosis.

127
Q

Essential tremor definition

A

Most commo type of tremor. Involuntary and rhythmic shaking, trembling often occurs in your hands, especially when you do simple tasks such as drinking from a glass or tying shoelaces.
Intention tremors are slower, zigzag-like movements which are evident during deliberate and visually guided movement.
Essential trmor can lead to trmors without accompanying intentional movements.

128
Q

Essential tremor risk facotrs

A

Advanced age, familial history, exposure to toxins.

129
Q

Essential tremor presentation

A

Usually absent at rest

130
Q

Essential tremor diagnosis

A

Clinical

131
Q

Essential tremor management

A

Propanolol, primidone

132
Q

Huntingdon’s disease definition

A

Autosomal dominant neurogenerative disorder

133
Q

Huntingdon’s disease pathophysiology

A

Expanded CAG repeat on huntingtin protein (chromosome 4) - toxic protein fragment production - cross-linking occurs - aggregation - resistance to degradation - interference with normal cellular function. Essentially, too much dopamine.

134
Q

Huntingdon’s disease presentation

A

Typical onset 35-45, more common northern europeans

Non-motor: irritability, impulsivity, personality change
Motor: main sign is hyperkinesia, chorea, twitching, loss of coordination

135
Q

Huntingdon’s disease diagnosis

A

Clinical diagnosis

MRI/CT - loss of striatal volume

136
Q

Huntingdon’s disease management

A

Non-pharmacological: counselling, carer support, physiotherapy, exercise

Pharmacological: antipsychotics, antidepressants, SSRIs dependent on symptoms

137
Q

Huntingdon’s disease complications

A

Prognosis is poor, concurrent disease and suicide are the most common causes of death

138
Q

Guillain-Barre syndrome definition

A

An acute immune-mediated demyelinating polyneuropathy. Immune response against peripheral nerve myelin. Most common cause of acute polyneuropathy.

139
Q

Guillain-Barre syndrome aetiology

A

Usually post-infective

  • campylobacter
  • EBV
  • CMV
  • mycoplasma
  • HIV

Antibodies attack nerves, symptoms present a few weeks after infection
Other causes include vaccination, surgery, trauma

140
Q

Guillain-Barre syndrome presentation

A

Progressive onset of distal limb weakness/numbness - symmetrical, ascending, TOES TO NOSE WEAKNESS
Absent tendon reflexes (LMN sign)
Sesnory deficit distally - paraesthesia
Respiratory/facial muscle involvement
Occasionally autonomic - HR/BP/urinary control

141
Q

Guillain-Barre syndrome diagnosis

A 
Bloods - B12, FBC, LFTs, TFTs 
Lumbar puncture 
- raised protein
- normal WCC
Spirometry and ECG for resp and cardiac functions respectively
142
Q

Guillain-Barre syndrome management

A 
IV Immunoglobulins for 5 days 
Plasma exchange (plasmapheresis) 
Avoid corticosteroids
143
Q

Lambert-Eaton syndrome definition

A

Lambert-Eaton myasthenic syndrome (LEMS) is an autoimmune disorder of the neuromuscular junction. Caused by impaired presynaptic release of ACh.
Autoimmune attack on presynaptic calcium channels.

144
Q

Lambert-Eaton syndrome aetiology

A

It occurs in association with an underlying cancer (CA-LEMS) (commonly small cell lung carcinoma) or without cancer and part of a more general autoimmune state (NCA-LEMS)

145
Q

Lambert-Eaton syndrome presentation

A

Insidious and gradual onset of fatigue, weakness and a dry mouth
Limb weakness - begins in the proximal legs, typically hip flexion and hip abdunction and subsequently usually affects the proximal arms
Weakness may lead to a ‘waddling gait’
Ptosis
Dysarthria, areflexia, ptosis, diplopia, impotence, dysphagia may be present

146
Q

Lambert-Eaton syndrome diagnosis

A

DDx: presents similarly to Myasthenia Gravis - check for ACh receptor antibodies to rule out MG
Nerve conduction studies, 50Hz
MRI for malignancy - 2yrs after diagnosis if cancer not already present

147
Q

Lambert-Eaton syndrome management

A

Acetylcholinesterase inhibitors

Amifampridine - improves muscle strength

Phase 2 Med (9 decks)

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