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3a Notes AC > Neuro 3a > Flashcards

Neuro 3a Flashcards

1
Q

AKA Mini stroke

Transient Ischaemic Attack

Crescendo TIA: 2 or more TIA in one week; Increases risk of stroke

A

Transient and reversible episode of sudden onset neurological dysfunction caused by ischemia, without acute infarction. Symptoms have generally fully resolved within 24 hours. But has the potential to cause pathological changes to brain

New definition below

Transient neurological dysfunction secondary to ischaemia without infarction.

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2
Q

Pathophysiology of TIA

Most common causes

A

Arterial emobolism or Thrombosis in a carotid, vertebral or cerebral artery.

Differentials: Until full recovery is made difficult to separate from stroke, hypoglycaemia, migraine aura, focal epilepsy

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3
Q

Signs And Symptoms of TIA

Sudden onset, focal neurological deficit but, rather than persisting, the features resolve, typically within 1 hour.

A

90% affect anterior circulation (carotid)

  • Hemipareisis
  • Hemi sensory disturbance
  • Dysphasia
  • Amaurosis Fugax (curtain over eyes)

10% affect the posterior circulation (Vertobrobasillar) - affecting brainstem

  • Loss of Consciousness
  • Bilateral motor disturbance
  • Homonymous Heminopia (can occur with anterior too, Diplopia
  • Dysarthria

Dysphasia: Disorder of language. Dysarthria: Disorder of speech

can also get ataxia, vertigo, or loss of balance

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4
Q

Causes of Amaurosis Fugax

Paiinless transient monocular visual loss – ‘a curtain coming down vertically into field of vision’.

A
  • Temporary reduction in the retinal, ophthalmic or ciliary artery blood flow, leading to retinal hypoxia.
  • This can be caused by atheromatous disease of the internal carotid/ophthalmic artery, vasospasm, optic neuropathies or vasculitis
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5
Q

What is Transient Global Amnesia post TIA?

A

Episodes of confusion/amnesia lasting several hours, followed by complete recovery.

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6
Q

What is Todd’s Paresis/Paralysis

A

Todd’s Paralysis (Focal weakness of body after seizure), Intracranial lesions (tumour, haematoma)

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7
Q

Diagnosis TIA

A
  • FBC, U&Es, Fasting lipid and glucose, ESR, LFT.
  • ECG to see AF or MI
  • Coagulation studies,
  • ECHO
  • Doppler USS of Carotids (assess for stenosis, if >70% offer carotid endarterectomy.
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8
Q

ABCD^2 post TIA

data from studies have suggested it performs poorly and it is therefore no longer recommended by NICE Clinical Knowledge Summaries

A

A — age >= 60, 1 point.
B — BP 140/90 mm Hg or greater, 1 point.
C — clinical features: unilateral weakness, 2 points; speech disturbance.
Without weakness, 1 point.
D — duration of symptoms: 60 minutes+, 2 points; 10–59 minutes, 1 point.
D — presence of diabetes: 1 point.
- An ABCD2 score of 4 or more. = RISK OF STROKE
- High risk Pts need specialist within 24h Low risk within 1wk

Advise not to drive for at least 4 weeks following a TIA.

Other High Risks:
– Atrial fibrillation.
– >1 TIA in one week.
– A TIA while on an anticoagulant.

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9
Q

Post TIA Management

A

Immediate
- Give aspirin 300 mg immediately
- Unless: Taking ant-coagulant, already taking low dose aspirin, Aspirin contraindicated
Long term
- Clopidogrel (Aspirin + dipyridamole if contraindicated) P2Y12 inhibitor
- Carotid artery endarterectomy if Carotid area stroke & if stenosis above 70%
- Add statin unless already taking one, aim to reduce HDL by 40%
## Footnote

If Patient has had crescendo TIA: Immediate Admission.
Suspected TIA in last 7 days: Urgent assesment within 24h
Suspected TIA >1week: Assesment within 7 days.

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10
Q

Investigations TIA

CT vs MRI Nice guidelines

A
  • CT brains should not be done ‘unless there is clinical suspicion of an alternative diagnosis that CT could detect’
  • MRI (including diffusion-weighted and blood-sensitive sequences) is preferred to determine the territory of ischaemia, or to detect haemorrhage or alternative pathologies
    it should be done on the same day as specialist assessment if possible
  • Urgent Carotid Doppler USS
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11
Q

Pathophysiology Stroke (CVA)

Ischaemic Vs Haemorrhagic

Stroke is the fourth largest cause of death in the UK

A
  • Ischaemic: Blockage in the blood vessel stops blood flow (85%). Thrombotic or Embolic
  • Haemorrhagic: (15%) Intracerebral haemorrhage or Subarachnoid.

fat air or clumps of bacteria may act as an emboli AF can lead to emboli

Haemorrhage can be caused by burst aneurysms

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12
Q

Risk Factors Stroke/TIA

A

age
hypertension
smoking
hyperlipidaemia (Ischemia)
diabetes mellitus (Ischemia)
anti coagulation therapy (haemorrhage)
COCP, vasculitis, polycythaemia, thrombophilia

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13
Q

Signs & Symptoms

Oxford Bamford Classification of Stroke

4 types

TACS, PACS, LACS, POCS

A

Total Anterior Circulation Stroke
1. Unilateral weakness of face, arm & leg
2. Homonymous Hemianopia
3. Higher Cerebral Dysfunction (Dysphasia, vasospatial disorder)
- Involves Middle & Anterior Cerebral arteries
Partial Anterior Circulation Stroke
- Two of the above
- Involves smaller arteries of anterior circulation e.g. upper or lower division of middle cerebral artery
Lacunar Syndrome
- arteries around the internal capsule, thalamus and basal ganglia presents with 1 of
1. unilateral weakness (and/or sensory deficit) of face and arm, arm and leg or all three.
2. pure sensory stroke.
3. ataxic hemiparesis
Posterior Circulation Syndrome
- vertebrobasilar arteries
- one of the following
1. Cerebellar or brainstem syndromes
2. loss of consciousness
3. isolated homonymous hemianopia

see other cards for other types

Others Lateral medullary syndrome (posterior inferior cerebellar artery) Brainstem infarction, Weber’s syndrome

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14
Q

Important in Anatomy

Different Types Of Strokes

8 Sites of Leisons

A

Anterior Cerebral Artery
- Contralateral hemipareisis, and sensory loss
- Lower extremity > Upper
Middle Cerebral Artery
- Contralateral hemipareisis, and sensory loss
- Upper extremity > Lower
- Homonymous Hemianopia
- Aphasia
Posterior Cerebral Artery
- Homonymous Hemianopia with macular sparing (due to MCA supplying blood)
- Visual Agnosia
Weber’s Syndrome
- Posterior Cerbreal Artery that supply midbrain
- Ipsilateral CN3 Palsy (eye may turn inward very slowly and may move only to the middle when looking inward. It cannot move up and down. eye lid droops)
- Contralateral weakness of upper and lower extremity
Wallenberg, Lateral Medullary Syndrome
- Posterior inferior cerebellar artery
- Ipsilateral: facial pain and temperature loss
- Contralateral: limb/torso pain and temperature loss
Ataxia, nystagmus
Anterior inferior cerebellar artery
- Same as above but ispilateral facial paralysis and deafness
Retinal Artery
- Amaurosis Fugax
Basillar Artery
- Locked in Syndrome

always factor in non dominance too.

Locked in is also known as pseudocoma, is a condition in which a patient is aware but cannot move or communicate verbally due to complete paralysis of nearly all voluntary muscles in the body except for vertical eye

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15
Q

Ischaemic Vs Haemorrhagic Stroke

A

Haemorrhages are more likely to have:

  • decrease in the level of consciousness: seen in up to 50% of patients with a haemorrhagic stroke
  • headache is also much more common in haemorrhagic stroke
  • nausea and vomiting is also common
  • seizures occur in up to 25% of patients
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16
Q

What is used to measure disability in Stroke

A

Disability is most commonly measured using the Barthel index (BI), an outcome measure for stroke

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17
Q

Investigations of Stroke

A

A non-contrast CT head scan is the first line radiological investigation for suspected stroke
one of the key questions to answer is whether there is an ischaemic stroke or haemorrhagic stroke. Rarely a third pathology such as a tumour may also be detected

ROSIER score

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18
Q

Management of Stroke

blood glucose, hydration, oxygen saturation and temperature should be maintained within normal limits
blood pressure should not be lowered in the acute phase unless there are complications e.g. Hypertensive encephalopathy*

A
  • 300mg Aspirin - for 2 wks (as soon as Haemorrhagic Stroke eliminated)
  • Thrombolysis within 4.5hr in Ischaemic (alteplase)
  • Thrombectomy within 6hrs with IV Thrombolysis - proximal anterior circulation
  • Thrombectomy for wake up strokes

Secondary Prevention

  • Clopidogrel (Aspirin + MR dipyridamole 2nd line) - lifelong

  • Anticoagulants should not be started until brain imaging has excluded haemorrhage, and usually not until 14 days have passed from the onset of an ischaemic stroke
  • if the cholesterol is > 3.5 mmol/l patients should be commenced on a statin.
    For Thrombectomy
  • NICE recommend a pre-stroke functional status of less than 3 on the modified Rankin scale and a score of more than 5 on the National Institutes of Health Stroke Scale (NIHSS)
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19
Q

Optic Tract Leisons From stroke & Symptoms

Homonymous Hemianopia

A

Homonymous hemianopia

Incongruous defects: lesion of optic tract
Congruous defects: lesion of optic radiation or occipital cortex
Macula sparing: lesion of occipital cortex

Homonymous quadrantanopias

Superior: lesion of the inferior optic radiations in the temporal lobe (Meyer’s loop)
Inferior: lesion of the superior optic radiations in the parietal lobe
Mnemonic = PITS (Parietal-Inferior, Temporal-Superior)

Bitemporal hemianopia

Lesion of optic chiasm
Upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
Lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

Congruous visual field defect is identical between the two eyes, whereas an incongruous defect differs in appearance between the eyes

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20
Q

Contraindications of Thrombolysis for Stroke Treatment

A

Absolute
- - Previous intracranial haemorrhage
- Seizure at onset of stroke
- Intracranial neoplasm
- Suspected subarachnoid haemorrhage
- Stroke or traumatic brain injury in preceding 3 months
- Lumbar puncture in preceding 7 days
- Gastrointestinal haemorrhage in preceding 3 weeks
- Active bleeding
- Pregnancy
- Oesophageal varices
- Uncontrolled hypertension >200/120mmHg
Relative
- Concurrent anticoagulation (INR >1.7)
- Haemorrhagic diathesis
- Active diabetic haemorrhagic retinopathy
- Suspected intracardiac thrombus
- Major surgery / trauma in the preceding 2 weeks

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21
Q

PAD OUT

Subarachnoid Haemorrhage Pathophysiology

Presence of blood within the space beetween arachnoid and pia mater

most common cause of SAH is head injury and this is called traumatic SAH . In the absence of trauma, SAH is termed spontaneous SAH

A
  • Intracranial berry aneurysm rupture (PCKD, Ehlers danlos) 85% cases
  • AV malformation
  • Myocytic aneurysm
  • Pituitary Apoplexy
  • LINKED TO POLYCYSTIC KIDNEY DISEASE
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22
Q

Subarachnoid Haemorrhage Symptoms

A
  • Thunder Clap Sudden Onset Headache
  • Nausea & Vomitting
  • Neck Stiffness & Phototobia (Meningism and Kernigs)
  • Hemiplegia, Seizures, coma, drowsiness
  • Papilledema
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23
Q

Subarachnoid Haemorrhage Investigations

A
  • CT: Hyperdense Star shape leison
  • Lumbar - if CT clear but suspicious, - 12H post symptoms (allows Breakdown) - looking for Xanthochromia (breakdown of Hb into Bilirubin giving a yellow colour)

Hyperdense=fresh blood.

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24
Q

Subarachnoid Haemorrhage Management & Complications.

A
  • Neurosurgery: Coil or Craniotomy with Clipping
  • Strict bed rest until treatment is finished
  • Vasospasm is prevented using a 21-day course of nimodipine
  • Hydrocephalus is temporarily treated with an external ventricular drain

Complications Below

  • Rebleeding (within first 12h)
  • Vasospassm
  • SIADH
  • Hydrocephalus
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25
Q

PAD OUT

Subdural Haematoma Pathophysiology

Collection of clotting blood in the subdural space (between arachnoid and dura mater)

A

Most commonly due to rupture of a vein
- tearing of bridging veins between the venous sinuses and the cortex
- usually due to deceleration injury during
violent head movement.
The accumulating haematoma causes raised ICP, shifting the midline structures.

RFs Below

Traumatic head injury; Cerebral atrophy/increasing age – makes bridging veins more vulnerable; Alcoholism (causes cerebral atrophy); Anticoagulation medication; Physical abuse in infant

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26
Q

Subdural Haematoma symptoms

Most commonly occur around the frontal and parietal lobes.

A

Interval between injury and symptoms span from days to months
Acute subdural haematoma
- Signs and symptoms of raised ICP (Headache, Nausea, Vomiting,
Raised BP)
- Confusion
- Seizure, Focal neurology
Chronic subdural haematoma
* cognitive decline, personality change, headache – may have no memory of initial trauma

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27
Q

Subdural Haematoma Investigations

A

CT gold standard Crescent shaped Mass, Goes from hyperdense to iso dense (same as brain) to hypo as clot ages
MRI useful to spot any other haematomas

  • Large acute subdural haematomas will push on the brain (‘mass effect’) and cause midline shift or herniation.

Infants also have fragile bridging veins and can rupture in shaken baby syndrome

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28
Q

Subdural Haematoma management & Complications

Complications: death, raised ICP -> Cerebral oedema

A

ABCDE
Refer to neurosurgery (craniotomy)
Mannitol for raised ICP

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29
Q

Common exam question on SDH

A

Elderly - Due to decrease in brain weight and increase in subdural space with increasing age, haematomas and symptoms evolve slowly. A common exam question will an elderly patient with progressive change in personality and
decreased GCS.

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30
Q

Extradural Haematoma Pathophysiology

Collection of clotting blood between dura mater and skull bone
Usually caused by injury.

A

Most commonly due to fracture of the temporal or parietal
bone causing laceration of the middle meningeal artery, typically after trauma to the temple. Blood accumulates rapidly over minutes-hours between the bone and Dura.

As the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebelli and the patient develops a fixed and dilated pupil due to the compression of the parasympathetic fibers of the third cranial nerve.

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31
Q

Extradural Haematoma Symptoms

Additional notes: Lucid interval – Time between Traumatic Brain injury and
Decrease in consciousness

A
  • Brief post-traumatic loss of consciousness
  • Lucid interval for several hours or even days, followed by altered consciousness
  • Severe headache, nausea and vomiting, confusion and seizures
  • Neurological deficit - contralateral hemiparesis, seizures
  • May lead to rapid Increase in Intra cranial pressure –ipsilateral pupillary dilatation, signs of brain stem compression and death
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32
Q

Extradural Haematoma Investigations

A

CT – gold standard Hyperdense Biconvex Lemon shape

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33
Q

Extradural Haematoma Management

A

ABCDE emergency management- assess and Stabilise the patient
Give Mannitol if increased ICP
Refer to Neurosurgeons - Craniotomy and clot evacuation/ Conservative Management

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34
Q

TTH Pathophysiology

A

The commonest primary headache.
episodic (<15 days/month)
chronic (>15 days a month for at least 3 months).
No organic cause

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35
Q

TTH Signs & symptoms

A

Bilateral, non-pulsatile, chronic daily headache: ‘tight-band like sensation’, pressure behind the eyes, mild-moderate pain
+/- scalp muscle tenderness
No vomiting, no sensitivity to head movement, no aura

not associated with aura, nausea/vomiting or aggravated by routine physical activity
may be related to stress
may co-exist with migraine

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36
Q

TTH investigations

A

Diagnosis
No Investigations, diagnosed based on clinical history.
Headache diaries may help (min 8 weeks)

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37
Q

TTH management

A

First line
aspirin, paracetamol or an NSAID are first-line
Second Line
Amytriptaline (TCA)
Prophylaxis
up to 10 sessions of acupuncture over 5-8 weeks

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38
Q

Medication Overuse Headaches

Management: simple analgesics and triptans should be withdrawn abruptly (may initially worsen headaches)
opioid analgesics should be gradually withdrawn

A
  • present for 15 days or more per month
  • developed or worsened whilst taking regular symptomatic medication
  • patients using opioids and triptans are at most risk
  • may be psychiatric co-morbidity

Beware Medication-Overuse Headaches – headache worsens whilst on regular analgesia, especially opioids

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39
Q

Migraine Pathophysiology

A
  • 3x more common in women
  • common triggers: alcohol, stress, tiredness, COCP, Cheese, Choc, Menstruation, Lights
    Theories
  • Neuronal hyperexcitability
  • Cortical spreading depolarisation
  • Activation of brainstem pain pathways and trigeminal neurons
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40
Q

Migraine Signs and Symptoms

A
  • Severe unilateral throbbing headache
  • nausea, phototobia, phonphobia (fear of sound)
  • 72h typical
  • Pts prefer dark quiet room
  • Aura in 1/3 of Pts (lasts 5-60mins before attack)
  • Hemianopic disturbance (vision)
  • aggravated by activity

Children: shorter headache time, GI disturbances

If Pt has motor weakness, visual symotoms of one eye, double vision, poor balance, delirious then refer to secondary care.

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41
Q

Migraine Hemiplegic

A
  • Weakness down one side of the body lasting 5min-24h simultaenous to migraine
  • Genetic component
  • Familial Hemiplegic Migraine
  • Important to rule out CVA or TIA
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42
Q

Migraine Management and other forms of migraine?

A
  • 1st line Sumatriptan (5HT agonist) + NSAID or Paracetamol
  • 2nd line; metoclopramide/prochlorperazine

Prophylactic (>2 incident P/M)
- Topiramate (teratogenic)
- Propranolol

Pregnancy
- Paracetamol 1st line
- NSAID 2nd line only in 1st+2nd Trimester
- Avoid aspirin and codeine

COC is contrainicated, risk of stroke

Menstruation try mefanamic acid or anadin combination paracetamol

for young Pt consider nasal triptan

if these measures fail NICE recommend ‘a course of up to 10 sessions of acupuncture over 5-8 weeks
- Riboflavin may help

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43
Q

Autosomal Dominant Link

Cluster Headaches Pathophysilogy & RFs

AKA

they typically occur in clusters lasting several weeks, with the clusters themselves typically once a year.

A
  • No known pathophysiology Unknown – theories include superficial temporal arterysmooth muscle hyper reactivity to 5HT
  • M:F 5:1
  • Smoking
  • alcohol may trigger an attack
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44
Q

Cluster Headache Symptoms

A
  • Rapid onset of excruciating pain around one eye
  • Rises to crescendo over minutes and lasts 15-160mins, once or twice/day
  • Nocturnal/early mornings – often wakes patient from sleep
  • Watery and bloodshot eye with lid swelling, lacrimation, facial flushing,rhinorrhoea,
  • miosis +/- ptosis (20% of the attacks)\
  • +/- vomiting
  • Can be chronic instead of episodic
  • Patient can be restless and agitated
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45
Q

Cluster Headache investigations and Management

A

Acute

  • High flow oxygen + triptan

Preventative

  • Verapamil
  • Some link to Predinslone

Avoid Alcohol during cluster period

Triptans to be avoided in patients with coronary artery disease history

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46
Q

Trigeminal Neuralgia Pathophysiology

Paroxysms of intense, debilitating pain in the distribution of the trigeminal nerve CNV
CNV is both sensory and motor- mostly it is the maxillary or mandibular branches

A
  • Compression of CNV from blood vessels leading to demylination & excitation of CNV = erratic pain signalling
  • Compression of the trigeminal roots by tumours another potential
  • More common in Females than Males
  • HTN risk factor
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47
Q

Trigeminal Neuralgia Symptoms

A
  • brief electric shock-like pains, abrupt in onset and termination, limited to one or more divisions of the trigeminal nerve
  • Lasts seconds to mins many times throughout day
  • Atypical CNV can cause burling like sensation

pain is commonly evoked by light touch, including washing, shaving, smoking, talking, and brushing the teeth (trigger factors), and frequently occurs spontaneously

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48
Q

Trigeminal Neuralgia Invesitgations and Management

Red Flags?

A
  • Carbamazepine is first-line
  • failure to respond to treatment or atypical features (e.g. < 50 years old) should prompt referral to neurology

Important to rule out Temporaral Arteritis

Red Flags

  • Sensory changes
  • Deafness or other ear problems
  • History of skin or oral lesions that could spread perineurally
  • Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
  • Optic neuritis
  • A family history of multiple sclerosis
  • Age of onset before 40 years
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49
Q

Giant Cell Arteritis (Temporal Arteritis) Pathophysiology

Temporal arteritis is large vessel vasculitis which overlaps with polymyalgia rheumatica (PMR). 50% cases

A
  • Inflammatory granulomatous vasculitis of larger cerebral arterites - commonly Temporal Artery.
  • typically patient > 60 years old
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50
Q

Giant Cell Arteritis (Temporal Arteritis) Signs and Symptoms

Common Pt: 60Year Old Male

A
  • Temporal pulsating headache
  • Scalp tenderness
  • Jaw claudication
  • Rapid Onset <1mth
  • anterior ischemic optic neuropathy (Posterior clliary artery) - Amaurosis Fugax
  • Systemic Features
  • Tender palpable temporal artery
  • Fundoscopy: Swollen pale disc + blurred margins

permanent visual loss is the most feared complication of temporal arteritis and may develop suddenly

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51
Q

Giant Cell Arteritis (Temporal Arteritis) Investigations and MAnagement

around 50% have features of PMR: aching, morning stiffness in proximal limb muscles (not weakness)

A
  • raised inflammatory markers
  • ESR > 50 mm/hr (note ESR < 30 in 10% of patients)
  • CRP may also be elevated
  • temporal artery biopsy: skip lesions may be present
    TREATMENT
  • Don’t delay starting of treatment - even before biopsyto prevent permamnent loss of sight
  • Giver high dose Prednislone - if no vision loss
  • Visual loss: IVmethylpredinslone
  • GIve PPI and Bisphosphonates as using long term steroids (12-18m)

there should be a dramatic response, if not the diagnosis should be reconsidered

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52
Q

Encephalitis Pathophysiology

A
  • Infection and Inflammation of the brain parenchyma
  • Often caused by HSV-1
  • Disease which mostly affects the frontal and temporal lobes - Focal signs, decreased consciousness.
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53
Q

Encephalitis Features

A
  • Viral infection symptoms
  • Focal feautres like aphasia
  • Progresses to decreases consciousness, drowsiness and confusion
  • Maybe even seizures

Cold sores doesnt matter.

Some may also exhibit signs of meningitis.

How well did you know this?
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54
Q

Encephalitis Investigations & Management

Permanent brain damage if left untreated.

A
  • CSF: lymohocytosis, elevated protein
  • PCR for HSV
  • Changes seen in neuroimaging (MRI)
  • EEG: 2Hz discharges
    Management
  • IV accyclovir high dose 14 days
55
Q

Meningitis Pathophysiology

Can be bacterial or Viral

A

Meningitis is an inflammation of the leptomeninges and the cerebrospinal fluid of the subarachnoid space.
- Viral more common than bacterial and self limiting.

56
Q

Meningitis RFs and Causes

A

Viral: HIV, Measels, Coxsackie virus, HSV
Bacterial
0-3mths - Group B Strep (acquired from mother), Ecoli, Listeria
3m-6y - Neisseria Meningitidis, Strep Pneumoniae, H. Influenzae
6y-60y - Neisseria Meningitidis (meningococcal), Strep Pneumoniae (pneumococcal)
>60Y - Strep Pneumonaie, Neisseria meningitidis, Listeria

Group B strep common in low birth wt, prolonged rupture of membranes

Meningococcal septicaemia is when it invades into blood, presence of endotoxin leads to inflammatory cascade. Petechial rash + signs of sepsis = meningococcal septicaemia

57
Q

Meningitis Signs and Symptoms

A
  • Fever
  • Headache – ‘Worse headache of life’ lasting minutes to hours
  • Meningism- Photophobia, neck stiffness (Kernigs and Brudzinski signs)
  • +/- Altered mental state (Due to cerebral oedema)
  • Seizures
  • NON-BLANCHING Petechial rash
58
Q

Viral & Bacterial

Meningitis Investigations

A
  • PCR and cultures
  • Lumbar puncture to asses CSF
    Viral: Raised Lymphocytes, Normal Protein and Glucose
    Bacterial: Polymorphs(neutrophils). Raised Protein, Low Glucose

Differentiate b/w TB and Bacterial: TB has lymphocytes instead of polys

The Ziehl-Neelsen stain is only 20% sensitive in the detection of tuberculous meningitis and therefore PCR is sometimes used (sensitivity = 75%)

59
Q

Viral and Bacterial

Meningitis Management

prophylaxis needs to be offered to household and close contacts of patients affected with meningococcal meningitis, if they have close contact within the 7 days before onset. For pneumococcal meningitis, no prophylaxis is generally needed.

A
  • Suspected Bacterial meningitis – Start Abx even before tests
  • Treatment: IV Cefotaxime (3rd Generation Cephalosporin) )
  • If in community e.g. GP, give IM Benzylpenincillin (meningicoccal)
    • Amoxicillin or Ampicillin (for under 3m or above 50) to cover Listeria
  • Prophylaxis – Rifampicin or Ciprofloxacin

Intravenous dexamethasone should also be given to reduce the risk of neurological sequelae, but the BNF advise to withhold if:
* septic shock
* meningococcal septicaemia
* immunocompromised
* meningitis following surgery

60
Q

Meningitis complications

A
  • Complications of meningitis include hearing loss, Seizures, and developmental problems
  • Cryptococcus Neoformans in HIV patients stains with India ink
  • Meningococcal disease is a notifiable disease (to health protection agency – HPA) in England and Wales.
61
Q

Guillain-Barre syndrome Pathophysiology

Miller Fisher syndrome
variant of Guillain-Barre syndrome
associated with ophthalmoplegia, areflexia and ataxia. The eye muscles are typically affected first

A
  • immune-mediated demyelination of the peripheral nervous system often triggered by an infection (classically Campylobacter jejuni)
  • infection causes production of antibodies, which then attack the body’s nerves myelin (molecular mimicry). Demyelination causes an acute polyneuropathy.
  • anti-GM1 antibodies
62
Q

Guillain-Barre syndrome
symptoms

Initial symptoms
around 65% of patients experience back/leg pain in the initial stages of the illness

A
  • Ascending (limbs first) progressive, symmetrical weakness +/- numbness of all the limbs.
  • reflexes are reduced or absent
  • sensory symptoms tend to be mild (e.g. distal paraesthesia) with very few sensory signs
  • May see Foot drop
  • History of Gastroenteritis or Resp infection
  • In 20%, respiratory muscles and facial muscles are affected ->respiratory involvement requires ITU admission

May also get Urinary retention, diarrhoea or Papilloedema

63
Q

Guillain-Barre syndrome Management and Investigations

A
  • admit to hospital for investigations
  • Confirmed with nerve conduction studies (decreased motor nerve velocity - prolonged distal motor latency)
  • Lumbar Puncture: +Proteins, WCC normal
  • IV immunoglobulin (IVIg) for 5 days: decreases duration and severity of paralysis.
64
Q

Epilepsy Pathophysioogy & RFs

Non Epileptic Seizures: Febrile convulsions. Alcohol Withdrawal (Delirium Tremens). Pseudo seizures (no electrical charge)

A
  • A recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain, manifesting as seizures.
  • Seizure is the clinical manifestation of dyssynchronous neuronal discharge.

Two types

1.) Primary Generalised: Bilaterally symmetrical and synchronous discharge involving both hemispheres, no focal brain abnormality.
2.) Focal: One hemisphere involved at onset. New onset focal seizures represent a focal structural abnormality until proven otherwise.

Epilepsy most commonly occurs in isolation
However it is also associated with:
* cerebral palsy: around 30% have epilepsy
* tuberous sclerosis
* mitochondrial diseases

65
Q

Symptoms of Epilepsy

Classification of Seizures

The basic classification of epilepsy has changed in recent years. The new basic seizure classification is based on 3 key features:
1. Where seizures begin in the brain
2. Level of awareness during a seizure (important as can affect safety during seizure)
3. Other features of seizures

A

Primary Generalised Consciousness lost from the start, involve both sides of brain.

  • Tonic Clonic (grand mal) Tonic phase (hypertonia, rigid, stiff limbs) to Clonic (generalised, bilateral, rhythmic jerking lasting from seconds to minutes, tongue bite and incontinence)
  • Clonic
  • Tonic
  • Typical Absence (impaired consciousness with mild or no motor involvement: patient will stop and stare for a few seconds – normal activity then resumed without awareness of seizure.
  • Myoclonic seizures (Shock like body jerks)
  • Atonic Seizures (Sudden brief loss of tone which may cause falls)

Focal Seizures Start in one specific area of brain

  • Focal Aware Seizure Awareness unimpaired with focal motor, sensory, autonomic or psychic symptoms. No post-ictal symptoms
  • Focal impaired Awareness - Alteration of consciousness (Loss of consciousness, automatisms, lip smacking, chewing, autonomic aura such as epigastric rising sensation)
  • Focal to bilateral (Focal Seizures that progress to generalised seizures)

Jacksonian movement: Clonic movements travelling proximally (frontal)

As well as the seizure activity described above patients who have had generalised seizures may
* bite their tongue
* experience incontinence of urine
* postictal phase where they feel drowsy and tired for around 15 minutes.

66
Q

Lobe Localising features in Epilpesy

A

TEMPORAL (head)

  • Hallucinations, Epigastric Rising, Automatisms, DejaVu

FRONTAL (motor)

  • Head/leg movements, posturing, post-ictal weakness, Jacksonian march

PARIETAL (sensory)

  • Parasthesia

OCCIPITAL (visual)

  • Floaters, Flashes

Automatisms (lip smacking/grabbing/plucking)
Jacksonian movement: Clonic movements travelling proximally (frontal)

67
Q

Investigations Epilepsy

A

Following their first seizure patients generally have both an

  • electroencephalogram (EEG)
  • neuroimaging (usually a MRI).

Clinical diagnosis: 2 unprovoked episodes occurring 24h apart

3Hz spike & wave seen in absence seizures

68
Q

Management Epilepsy

Driving Guidance?

maternal use of sodium valproate is associated with a significant risk of neurodevelopmental delay in children fine in breastfeeding

A

Tonic Clonic/Tonic/Atonic: Sodium Valp in M. Lamotrigine in F (U10 F offer Valp 1st line)
Focal: Lamotrigine - 2nd line: Carbamazepine
Absence: Ethosuximide 2nd line: same as tonic clonic
Myoclonic: M: Sodium Valp. F: Levetiracetam

generally patients cannot drive for 6 months following a seizure

Driving Guidance

  • Seizure free for 6m non-epileptic diagnosis
  • Seizure Free for 12m for epileptic diagnosis

Gyne Advice

  • All women thinking about becoming pregnant should be advised to take folic acid 5mg per day well before pregnancy to minimise the risk of neural tube defects.
  • Contraception For women taking phenytoin,carbamazepine, barbiturates, primidone, topiramate, oxcarbazepine:
    UKMEC 3: the COCP and POP
    UKMEC 2: implant
    UKMEC 1: Depo-Provera, IUD, IUS
69
Q

Complications in Epilepsy

+ side effect profiles of meds used

A

Status epilepticus – (Seizure lasting >30 mins) medical emergency.

  • ABCDE
  • Check glucose
  • Rectal Diazepam or IV lorazepam x2
  • If ongoing (or ‘established’) status it is appropriate to start a second-line agent such as phenytoin or phenobarbital infusion
  • If no relief then intubate.

SUDEP - Sudden unexpected death in epilepsy. Death of patient with epilepsy put down to status epilepticus.

prehospital setting PR diazepam or buccal midazolam

Na Valp: Wt gain, alopecia, ataxia, tremor, teratogenic
Carbamazepine: Diziness, ataxia, leucopenia
Lamotrigine: Stevens Johnson Syndrome
Phenytoin: Osteomalaxia, brith defects, diziness, ataxia.

70
Q

Parkinson’s Disease Pathophysiology

degenerative movement disorder

  • around twice as common in men
  • mean age of diagnosis is 65 years
A
  • degeneration of dopaminergic neurons in the substantia nigra - basal ganglia
  • Developments of Lewy-Bodys: Ubiquitin, alpha synuclein
  • Loss of dopamine and melanin in striatum -> akinesia
  • Symptoms of Parkinson’s disease are characteristically asymmetrical.

Akinesia: loss of voluntary movements.

71
Q

Essential Vs Intention Vs Resting Tremor

Resting (pill rolling) seen in Parkinsons

A

Intention tremor on movement refers to cerebellar disorder, Cerebellar signs e.g. Past-pointing, nystagmus etc
Essential tremor A.Dominant condition affecting both upper limbs, treated with beta blockers, worse when arm are stretched out
Resting Tremor: common in Parkinsons, gets better with movement, often unilateral

72
Q

The onset of symptoms is insidious

Parkinson’s Symptoms

Triad

Drug-induced parkinsonism has slightly different features to Parkinson’s disease:
motor symptoms are generally rapid onset and bilateral
rigidity and rest tremor are uncommon

A
  1. Bradykinesia; short shuffling steps with reduced arm swinging
  2. Tremor; most marked at rest, improves with movement. Pill rolling
  3. Rigidity; lead pipe, cogwheel

depression common with postural hypotension

Fine movement difficulty,
Cog wheeling, parkinsonian gait, postural instability leading
to falls, micrographia, brisk reflexes, mask like face.

73
Q

Parkinson’s Management

Diagnosis is clinical
Confirm with response to levodopa
MRI will show atrophy but not initially

A
  • Motor Symptoms: Levodopa (Co-Carbidopa)
  • Non-motor symptoms: MAO-B inhibs (selegiline, rasagiline) or Levodopa
  • Dopamine Agonists (initial therapy before levodopa) ropinirole - Doesn’t really help motor symptoms
  • Symptoms despite optimal levodopa treatment or has developed dyskinesia then NICE recommend the addition of a dopamine agonist, MAO‑B inhibitor or catechol‑O‑methyl transferase (COMT) inhibitor as an adjunct. Entacapone, tolcapone

MAO-B inihib breakdown of dopamine

the risk of acute akinesia or neuroleptic malignant syndrome if medication is not taken/absorbed (for example due to gastroenteritis)

74
Q

LEVODOPA

common adverse effects:

  • dry mouth
  • anorexia
  • palpitations
  • postural hypotension
  • psychosis
A

Levodopa is a precursor to dopamine, but dopamine cannot cross the blood brain barrier whereas L-Dopa can. The decarboxylase inhibitor prevents peripheral conversion of L-dopa to dopamine, and therefore reduces the peripheral side effects of nausea and vomiting, arrhythmias, alopecia and hypotension. Note – Levodopa DOES NOT alter disease progression, it just offers symptom relief

never acutely stop levodopa.

Limitations of levodopa: Reduced efficacy over time, even with increasing dose, L-dopa induced dyskinesia, On-off effect: fluctuations in motor performance

75
Q

Huntington’s Disease Pathophysiology

  • Autosomal dominant
  • progressive neurodegenerative disorder.
  • The mean age of onset is 30-50 years.
A
  • Mutation Chromsome 4 - CAG repeats
  • More CAG repeats in body the quicker the onset
  • Cerebral atrophy
  • Loss of neurones in caudate nucleus and basal ganglia
  • Decreased ACh synthesis and GABA in striatum. Normal dopamine levels.
76
Q

Huntington’s Disease Signs & Symptoms

Prodromal: relating to or denoting the period between the appearance of initial symptoms and the full development of a rash or fever.

A
  • Often a prodromal phase of mild psychotic and behavioural symptoms
  • development of chorea (uncontrolled movement)
  • This may begin as general restlessness, unintentionally initiated movements, lack of coordination and slow saccadic eye movements
  • Progresses to rigidity, writhing and abnormal posture
  • Dysarthria, dysphagia and abnormal eye movements are common.
  • Behavioural change: aggression, addictive behaviour, depression/anxiety, apathy, self-neglect

Chorea: - Relentlessly progressive, jerky, explosive, figidity movements

Dementia: impaired cognitive abilities and memory
It is also frequently associated with seizures. Late features include spasticity, clonus, supranuclear gaze palsy and extensor plantar, and death generally occurs within 15 years of diagnosis, usually from an intercurrent illness e.g. infection

77
Q

Huntington’s Disease Investigations and management

A
  • Clinical Diagnosis
  • CT/MRI will show caudate nucleus atrophy, and increased size of atrophy and increased of the frontal horns of the lateral ventricles
  • There is no treatment to prevent progression.
  • Symptomatic management of chorea: benzodiazepines, valproic acid, tetrabenazine (dopamine depleting agent)

Counselling to patient and family, genetic counselling to any children of the patient.

78
Q

Motor Neurone Disease Pathophysiology

UMN or LMN or BOTH

A
  • A sporadic or hereditary (10%) disease affecting upper and/or lower motor neurones
  • Characterised by progressive degeneration of motor neurone in the spinal cord (anterior horns), cranial nerve motor nuclei and within the cortex

RFs
Genetic (10%) – genes involved: C9ORF72, SOD1, TDP43, FUS; But primarily sporadic and unknown trigger.

79
Q

Motor Neurone Disease Types

4 types

A
  1. Amyotrophic Lateral Sclerosis: LMN in arms UMN in legs, most common, chromosome 21 link.
  2. Primary Lateral Sclerosis: UMN
  3. Progressive Muscular Atrophy: LMN, Distal before Proximal, Best prognosis
  4. Progressive Bulbar Palsy: UMN & LMN Palsy of tongue, swallowing, chewing, facial muscles, worst prognosis

Regardless of the body part that is first affected by ALS disease, weakness and atrophy spread to other parts of body with varying degrees of upper motor neuron (UMN) symptoms (e.g., spasticity) and eventually involve the muscles of all 4 extremities and the trunk, as well as bulbar muscles.

80
Q

UMN vs LMN

A

UMN
- Weakness
- Brisk Reflexes
- Hypertonia
- Upgoing Plantars (Babinski +ve)
- Clonus

LMN
* Weakness
* Absent Reflexes
* Hypotonia
* Wasting
* Fasiculations

81
Q

Motor Neurone Disease general Symptoms

A
  • fasciculations
  • the absence of sensory signs/symptoms
  • the mixture of lower motor neuron and upper motor neuron signs
  • wasting of the small hand muscles/tibialis anterior is common

  • doesn’t affect external ocular muscles
  • no cerebellar signs
  • abdominal reflexes are usually preserved and sphincter dysfunction if present is a late feature
82
Q

Motor Neurone Disease Management

A
  • Diagnosis based on clinical findings and EMG/nerve conduction
  • Riluzole - Glutamate antagonist - used in ALS
  • Sometimes BIPAP used in night (respiratory care-non invasive)

Poor prognosis, many Pts die within 3 years

percutaneous gastrostomy tube (PEG) is the preferred way to support nutrition and has been associated with prolonged survival

83
Q

Multiple Sclerosis Pathophysiology

A chronic inflammatory disorder of the Central Nervous System associated with progressive disability

A
  • More common in Whites & Females
  • Link to previous infection of EBV, MMR
  • Immune-mediated demyelination at multiple CNS sites occurs as discrete plaques.
  • T-cell mediated: T cells activate B cells to produce auto-antibodies against myelin. Repeat demyelination leads to axonal loss and incomplete recovery between attacks, destroying oligodendrocytes
84
Q

Subtypes of Multiple Sclerosis

A
  1. Relapsing Remitting - Most common Type
  2. Secondary Progressive MS - Start with Relaps & Remit with Worsening symptoms eventually no remission
  3. Primary Progressive MS - Gradually getting worse over time no remission

Patients usually die from aspiration pneumonia 15y before average age of death.

84
Q

Multiple Sclerosis Signs & Symptoms

A

Visual

  • Optic Neuritis - Uhtoffs (Worsening of vision with raised temperature)
  • Optic Atrophy
  • Internuclear opthalmoplegia

Sensory

  • Pins and Needles
  • Numbness
  • Trigeminal Neuralgia
  • Lhermittes: Parasthesia in Limbs on neck flexion

Motor

  • Spasms in Legs

Cerebellar

  • Ataxia: often seen in acute relapse
  • Tremor

Others: urinary inconitence, Sexual Dysfunction, Intelectual deterioration

85
Q

Multiple Sclerosis Diagnosis & Treatment

Treatment in multiple sclerosis is focused on reducing the frequency and duration of relapses. There is no cure.

A

Diagnosis

  • MRI with contrast should be used to view demyelinating lesions such as MS

Acute Relapse

  • 5 days Oral/IV methylpredinslone

Realpse Prevention

  • IV Natalizumab, Ocrelizumab
  • Finolimod
  • Beta Interferon SC/IM

Spasticity
baclofen and gabapentin are first-line. Other options include diazepam, dantrolene and tizanidine
physiotherapy is important
cannabis and botox are undergoing evaluation

Bladder dysfunction
may take the form of urgency, incontinence, overflow etc
guidelines stress the importance of getting an ultrasound first to assess bladder emptying - anticholinergics may worsen symptoms in some patients
if significant residual volume → intermittent self-catheterisation
if no significant residual volume → anticholinergics may improve urinary frequency

Oscillopsia (visual fields appear to oscillate)
gabapentin is first-line

86
Q

Define the concept of anticipation

Seen in Huntington’s Disease

A

Huntington’s chorea displays something called genetic “anticipation”. Anticipation is a feature of trinucleotide repeat disorders. This is where successive generations have more repeats in the gene, resulting in:

  • Earlier age of onset
  • Increased severity of disease
87
Q

Myasthenia Gravis Pathophysiology

Autoimmune disorder affecting Neuro Muscular Junction involving Ach

Associations
thymomas in 15%
autoimmune disorders: pernicious anaemia, autoimmune thyroid disorders, rheumatoid, SLE
thymic hyperplasia in 50-70%

A

An autoimmune disease mediated by antibodies against nicotinic acetylcholine receptors (AChR); this interferes with neuromuscular transmission via depletion of working post synaptic receptors. Immune complexes of AChR IgG and complement are deposited at the post synaptic membrane

More common in women

88
Q

Myasthenia Gravis Signs and Symptoms

A
  • Muscle Fatigueabilty
  • extraocular muscle weakness: diplopia
  • proximal muscle weakness: face, neck, limb girdle
  • ptosis
  • dysphagia

Diplopia: Double Vision Ptosis: Droopy eyelid Dysphagia: Struggle to swallow

89
Q

Myasthenia Gravis Investigations

A
  • Electromyography
  • CT thorax to exclude thyoma
  • AchR antibodies
  • Tensilon test (not commonly used due to risk of Cardiac Arrythmias)
90
Q

Myasthenia Gravis Treatment

A
  • Pyridostigmine (Ach inhib)
  • Prednislone, azathioprine, cyclosporine
  • Thymectomy

Management of myasthenic crisis

  • plasmapheresis
  • intravenous immunoglobulins
91
Q

Glioblastoma Multiforme

Side note: Metastatic Brain cancer is most common form of brain tumour (untreatable) - lung most common, breast and bowel included.
- 60% = Glioma and metastatic disease
- 20% = Meningioma
- 10% = Pituitary lesions

A
  • Most common primary tumour
  • poor prognosis: 1y
  • solid tumour with central necrosis - disrupt BBB = vasogenic oedema
  • Postoperative chemo/radio therapy.
  • Dexamethasone for the oedema
92
Q

Meningioma

2nd most common

A
  • from the arachnoid cap cells of the meninges and are typically located next to the dura and cause symptoms by compression rather than invasion.
  • Radiotherapy of Surgical resection
93
Q

VIII Crainial nerve

Vestibular Schwannoma

(previously termed acoustic neuroma)

A

It presents with

  • hearing loss
  • facial nerve palsy
  • Tinnitus
    Antoni A or B patterns seen
    Treatment radiotherapy and/or surgery

Neurofibromatosis type 2 is associated with bilateral vestibular schwannomas.

94
Q

Pilocytic Astrocytoma

A
  • Most common Primary tumour in children
  • Rosenthal Fibres
95
Q

Medulloblastoma

A

aggressive paediatric brain tumour that arises within the infratentorial compartment. It spreads through the CSF system.

  • Treat with surgical resection and chemotherapy

In paediatric practice medulloblastomas (neuroectodermal tumours) were the commonest lesions, astrocytomas now account for the majority.

96
Q

Ependyoma

A
  • Commonly seen in the 4th ventricle
  • May cause hydrocephalus
  • Histology: perivascular pseudorosettes
97
Q

Oligodendroma

A
  • Benign, slow-growing tumour common in the frontal lobes
  • Histology: Calcifications with ‘fried-egg’ appearance
98
Q

Haemangioblastoma

A
  • Tumour of the Cerebellum
  • Associated with von-Hippel-Lindau syndrome
99
Q

Pituitary adenoma

Secretory (produce hormone in excess) Non-secretory

A
  • Patients will present with the consequences of hormone excess (e.g. Cushing’s due to ACTH, or acromegaly due to GH) or depletion. Compression of the optic chiasm will cause a bitemporal hemianopia due to the crossing nasal fibers.
  • Investigation requires a pituitary blood profile and MRI. Treatment can either be hormonal or surgical (e.g. transphenoidal resection).
100
Q

Crainopharyngioma

A
  • Most common paediatric supratentorial tumour
  • Present with hormonal disturbance, hydrocephalus, bitemporal hemianopia
  • Derived from remnants of Rathke pouch

Can also present in adulthood

101
Q

Herpes Simplex Encephalitis

The virus characteristically affects the temporal lobes

Pathophysiology

  • HSV-1 is responsible for 95% of cases in adults
  • typically affects temporal and inferior frontal lobes
A

Features

  • fever, headache, psychiatric symptoms, seizures, vomiting
  • focal features e.g. aphasia
  • peripheral lesions (e.g. cold sores) have no relation to the presence of HSV encephalitis

INVESTIGATIONS
- CSF: Lymphocytosis. Elevated protein
- CT: temporal and frontal changes
Treatment
- IV Accyclovir

102
Q

Syncope

Three types: Reflex, Cardiac, Orthostatic

defined as a transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery

A

Reflex syncope (neurally mediated)

  • vasovagal: triggered by emotion, pain or stress. Often referred to as ‘fainting’
  • situational: cough, micturition, gastrointestinal
  • carotid sinus syncope

Orthostatic syncope

  • primary autonomic failure: Parkinson’s disease, Lewy body dementia
  • secondary autonomic failure: e.g. Diabetic neuropathy, amyloidosis, uraemia
  • drug-induced: diuretics, alcohol, vasodilators
  • volume depletion: haemorrhage, diarrhoea

Cardiac syncope

  • arrhythmias: bradycardias (sinus node dysfunction, AV conduction disorders) or tachycardias (supraventricular, ventricular)
  • structural: valvular, myocardial infarction, hypertrophic obstructive cardiomyopathy
  • others: pulmonary embolism

Reflex syncope is the most common cause in all age groups

Evaluation
cardiovascular examination
postural blood pressure readings: a symptomatic fall in systolic BP > 20 mmHg or diastolic BP > 10 mmHg or decrease in systolic BP < 90 mmHg is considered diagnostic
ECG
carotid sinus massage
tilt table test
24 hour ECG

103
Q

may also occur independently as an autoimmune disorder

Lambert Eaton Syndrome Features

seen in association with small cell lung cancer& breast& ovarian cancer.

A
  • Caused by an antibody directed against presynaptic voltage-gated calcium channel in the peripheral nervous system.
  • repeated muscle contractions lead to increased muscle strength (in contrast to myasthenia gravis)
  • Lower limb girdle weakness
  • hypo reflexia, dry mouth, impotence, difficulty urinating

Treatment

  • treat underlying cancer
  • Immunosupression with Prednislone or azathioprine
  • IV immunoglobulin and plasma exchange may be beneficial.
104
Q

most common hereditary peripheral neuropathy

Charcot Marie Tooth Syndrome

results in a predominantly motor loss.

A
  • There may be a history of frequently sprained ankles
  • Foot drop
  • High-arched feet (pes cavus)
  • Hammer toes
  • Distal muscle weakness
  • Distal muscle atrophy
  • Hyporeflexia
  • Stork leg deformity
105
Q

Cerebellar Syndrome

Unilateral cerebellar lesions cause ipsilateral signs.

Useful and well-known mnemonic to remember symptoms of cerebellar disease is DANISH:

A

D - Dysdiadochokinesia, Dysmetria (past-pointing), patients may appear ‘Drunk’
A - Ataxia (limb, truncal)
N - Nystamus (horizontal = ipsilateral hemisphere)
I - Intention tremour
S - Slurred staccato speech, Scanning dysarthria
H - Hypotonia

Causes

  • Friedreich’s ataxia, ataxic telangiectasia
  • neoplastic: cerebellar haemangioma
  • stroke
  • alcohol
  • multiple sclerosis
  • hypothyroidism
  • drugs: phenytoin, lead poisoning
  • paraneoplastic e.g. secondary to lung cancer
106
Q

Peripheral Neuropathies

divided into motor or sensory loss

A

Motor
- GBS
- Porphyria
- Lead poisoning
- Charcot Marie Tooth
Sensory
- Diabetes
- Uraemia
- Leprosy
- Vit B12
- Amyloidosis
- Alcholosm

Alcoholic neuropathy
secondary to both direct toxic effects and reduced absorption of B vitamins
sensory symptoms typically present prior to motor symptoms

Vitamin B12 deficiency
subacute combined degeneration of spinal cord
dorsal column usually affected first (joint position, vibration) prior to distal paraesthesia

Drugs causing a peripheral neuropathy
amiodarone
isoniazid
vincristine
nitrofurantoin
metronidazole

107
Q

Cranial Nerves (Palsies)

some say marry money but my brother says big boobs matter most

I: Olfactory II: Optic III:Occulomotor IV: Trochlear V: Trigeminal VI: Abducens VII:Facial VIII:Vestibulocochlear IX:Glosopharyngeal X:Vagus XI:Accessory XII: Hypoglosaal

A

I: Olfactory: Smell
II: Optic: Sight
III: Occulomotor: Fixed pupil (dilated), down and out eye, Ptosis
IV: Trochlear: Downward Gaze, Vertical Diplopia, vision worse when going down stair
V: Trigeminal: Neuralgia, Loss corneal Reflex, loss sensation (facial), Unable to masticate muscles, deviation of jaw to weak side
VI: Abducens: Horizontal Diplopia due defection abduction
VII: Facial: Flaccid paralysis of upper and lower face, loss of corneal reflex, loss of taste, hyperacusis
VIII: Vestibulocochlear: Hearing loss, vertigo, acoustic neuroma
IX: Glosopharyngeal: Hypersensitive carotid sinus reflex, loss of gag refelx
X: Vagus: Uvula deviation, loss of gag reflex
XI: Accessory: weakness turning head to contralateral side
XII: Hypoglossal: tonge deviates from site of leison

Abduction: moving away

  • Raised ICP can caused 3rd nerve palsy due to herniation, common also with posterior communicating artery aneurysm.
108
Q

Crainial Nerve reflexes

6

A
  1. corneal: 5 & 7
  2. Jaw Jerk: 5
  3. Gag: 9&10
  4. Carotid Sinus 9 & 10
  5. Pupillary Light: 2 and 3
  6. Lacrimation: 5 and 7
109
Q

Supply - ‘face, ear, taste, tear’

Facial nerve palsy

CN: 7

VII: Facial: Flaccid paralysis of upper and lower face, loss of corneal reflex, loss of taste, hyperacusis

A

LMN vs. UMN
upper motor neuron lesion ‘spares’ upper face i.e. forehead
lower motor neuron lesion affects all facial muscles
LMN:

  • Bell’s palsy
  • Ramsay-Hunt syndrome (due to herpes zoster)
  • acoustic neuroma
  • parotid tumours
  • HIV
  • multiple sclerosis
  • diabetes mellitus

UMN:

  • Stroke
110
Q

Bell’s Palsy

LMN

acute, unilateral, idiopathic, facial nerve paralysis. of unknown aetiology. common in pregnant women.

A
  • lower motor neuron facial nerve palsy - forehead affected
  • patients may also notice post-auricular pain (may precede paralysis), altered taste, dry eyes, hyperacusis
  • oral prednisolone within 72 hours of onset of Bell’s palsy
  • paralysis shows no sign of improvement after 3 weeks, refer urgently to ENT
  • most people with Bell’s palsy make a full recovery within 3-4 months

eye care is important to prevent exposure keratopathy

if untreated around 15% of patients have permanent moderate to severe weakness

111
Q

Important Dermatomes

A

c6: Thumb index finger
C7: Middle finger and palm
C8(T1): Ring and little finger
T10: umbilcus
L4: knee cap
L5: Largest toe
S1: Lateral foot and smallest toe
S2+S23: Genitalia

Erb-Duchenne paralysis
damage to C5,6 roots
winged scapula
may be caused by a breech presentation

Klumpke’s paralysis
damage to T1
loss of intrinsic hand muscles
due to traction

Foot drop
The sciatic nerve divides into the tibial and common peroneal nerves. Injury often occurs at the neck of the fibula
weakness of the foot dorsiflexors. weakness of foot eversion
A common peroneal nerve lesion is the most common cause

112
Q

Shingles

virus lies dormant in the dorsal root or cranial nerve ganglia.

acute, unilateral, painful blistering rash caused by reactivation of the varicella-zoster virus (VZV).

A

RF: Age, HIV, Immunocompromised
Commonly affects T1-L2
Symptoms: Burning pain 2-3 days, Headache, lethargy, erythematous, macular rash which becomes vesicular, demarcated by dermatome and doesnt cross the midline
Treatment: Antivrals within 72h. oral corticosteroids may be considered in the first 2 weeks. paracetamol and NSAIDs are first-line as analgesia

Remind patient their infectiousand avoid pregnant women and the ill

one of the benefits of prescribing antivirals is a reduced incidence of post-herpetic neuralgia, particularly in older people

Complication: Ramsay Hunt syndrome with can affect facial nerve

113
Q

Median Nerve Damage

A

Damage at wrist

    • e.g. carpal tunnel syndrome
    • paralysis and wasting of thenar eminence muscles and opponens pollicis (ape hand deformity)
    • sensory loss to palmar aspect of lateral (radial) 2 ½ fingers

Damage at elbow, as above plus:

  • unable to pronate forearm
  • weak wrist flexion
  • ulnar deviation of wrist

Anterior interosseous nerve (branch of median nerve)

  • leaves just below the elbow
  • results in loss of pronation of forearm and weakness of long flexors of thumb and index finger

Carpal tunnel Syndrome: caused by compression of median nerve in the carpal tunnel

pain/pins and needles in thumb, index, middle finger
Examination
* weakness of thumb abduction (abductor pollicis brevis)
* wasting of thenar eminence (NOT hypothenar)
* Tinel’s sign: tapping causes paraesthesia
* Phalen’s sign: flexion of wrist causes symptoms
* * Prolongation of Action Potential
* NICE Clinical Knowledge Summaries currently recommends a 6-week trial of conservative treatments if moderate then corticosteroid injection or wrist splints at night.
* Conservative management surgical decompression of flexor retinaculum.

114
Q

Radial Nerve Damage

A

Patterns of damage
* wrist drop
* sensory loss to small area between the dorsal aspect of the 1st and 2nd metacarpals

Axillary damage
* as above
* paralysis of triceps

115
Q

Ulnar Nerve Damage

A

Damage at wrist
‘claw hand’ - hyperextension of the metacarpophalangeal joints and flexion at the distal and proximal interphalangeal joints of the 4th and 5th digits
wasting and paralysis of intrinsic hand muscles (except lateral two lumbricals)
wasting and paralysis of hypothenar muscles
sensory loss to the medial 1 1/2 fingers (palmar and dorsal aspects)

Damage at elbow
as above (however, ulnar paradox - clawing is more severe in distal lesions)
radial deviation of wrist

116
Q

Narcolepsy

Typical onset in teenage years.

  • associated with HLA-DR2
  • it is associated with low levels of orexin (hypocretin), a protein which is responsible for controlling appetite and sleep patterns
A
  • hypersomnolence (recurrent episodes of excessive daytime sleepiness or prolonged nighttime sleep)
  • cataplexy (sudden loss of muscle tone often triggered by emotion - Buckling knees to collapse)
  • sleep paralysis
  • vivid hallucinations on going to sleep or waking up

Investigation

  • multiple sleep latency EEG

Management

  • daytime stimulants (e.g. modafinil) and nighttime sodium oxybate
117
Q

Triad of Symptoms

Normal Pressure Hydrocephlaus

Could be secondary to reduced CSF absorption at the arachnoiod villi

reversible cause of dementia seen in elderly patients. It is thought to be secondary to reduced CSF absorption at the arachnoid villi.

A
  1. Urinary incontinence
  2. Dementia and bradyphrenia (slow thought)
  3. gait abnormality (may be similar to Parkinson’s disease)
  • 60% of patients will have all 3 features at the time of diagnosis.
  • ventriculomegaly in the absence of, or out of proportion to, sulcal enlargement
  • Management ventriculoperitoneal shunting
  • around 10% of patients who have shunts experience significant complications such as seizures, infection and intracerebral haemorrhages.

bradyphrenia: slowed thinking and processing of information

118
Q

Hydrocephalus

RAISED Intracranial pressure

condition in which there is an excessive volume of cerebrospinal (CSF) fluid within the ventricular system of the brain and is caused by an imbalance between CSF production and absorption.

A
  • Headache (typically worse in the morning, when lying down and during valsalva)
  • Nausea and vomiting
  • Papilloedema
  • Coma (in severe cases)
  • CT head is used as a first line imaging investigation since it is fast and shows adequate resolution of the brain and ventricles
  • Lumbar puncture is both diagnostic and therapeutic since it allows you to sample CSF, measure the opening pressure, but also to drain CSF to reduce the pressure
  • An external ventricular drain (EVD) is used in acute, severe hydrocephalus and is typically inserted into the right lateral ventricle and drains into a bag at the bedside
  • A ventriculoperitoneal shunt (VPS) is a long-term CSF diversion technique that drains CSF from the ventricles to the peritoneum
  • In obstructive hydrocephalus, the treatment may involve surgically treating the obstructing pathology

Obstructive hydrocephalus is due to a structural pathology blocking the flow of cerebrospinal fluid. Dilatation of the ventricular system is seen superior to site of obstruction. Causes include: tumours, acute haemorrhage (e.g. subarachnoid haemorrhage or intraventricular haemorrhage) and developmental abnormalities (e.g. aqueduct stenosis). **Do not use Lumbar puncture in obstructive)

Non-obstructive hydrocephalus is due to an imbalance of CSF production absorption. It is either caused by an increased production of CSF (e.g. choroid plexus tumour (very rare)) or more commonly a failure of reabsorption at the arachnoid granulations (e.g. meningitis or post-haemorrhagic).

119
Q

Neurofibromatosis

There are two types of neurofibromatosis, NF1 and NF2. Both are inherited in an autosomal dominant fashion

A

NF1 is also known as von Recklinghausen’s syndrome. It is caused by a gene mutation on chromosome 17 which encodes neurofibromin and affects around 1 in 4,000

    • Café-au-lait spots (>= 6, 15 mm in diameter)
  • Axillary/groin freckles
  • Peripheral neurofibromas
  • Iris hamatomas (Lisch nodules) in > 90%
  • Scoliosis
  • Pheochromocytomas

NF2 is caused by gene mutation on chromosome 22 and affects around 1 in 100,000

  • Bilateral vestibular schwannomas
  • Multiple intracranial schwannomas, mengiomas and ependymomas
120
Q

Brain Abscess

The presenting symptoms will depend upon the site of the abscess

number of causes including, extension of sepsis from middle ear or sinuses, trauma or surgery to the scalp, penetrating head injuries and embolic events from endocarditis

A

headache

  • often dull, persistent
    fever
  • may be absent and usually not the swinging pyrexia seen with abscesses at other sites

focal neurology

  • e.g. oculomotor nerve palsy or abducens nerve palsy secondary to raised

intracranial pressure
other features consistent with raised intracranial pressure

  • nausea
  • papilloedema
  • seizures

surgery
a craniotomy is performed and the abscess cavity debrided
the abscess may reform because the head is closed following abscess drainage.
IV antibiotics: IV 3rd-generation cephalosporin + metronidazole
intracranial pressure management: e.g. dexamethasone

121
Q

found by the ‘swinging light test’

Relative afferent pupillary defect

Marcus-Gunn pupil

A
  • caused by a lesion anterior to the optic chiasm i.e. optic nerve or retina
  • the affected and normal eye appears to dilate when light is shone on the affected
  • MRI with contrast used for diagnosis of optic neuritis

Causes
retina: detachment
optic nerve: optic neuritis e.g. multiple sclerosis

122
Q

Glaucoma

Glaucomas are optic neuropathies associated with raised intraocular pressure (IOP).

A
  • increased intraocular pressure
  • visual field defect
  • pathological cupping of the optic disc1

Investigation
- slit lamp examination with pupil dilatation to assess optic neve and fundus for a baseline
- applanation tonometry to measure IOP

Management

  • first line: prostaglandin analogue (PGA) eyedrop
  • second line: beta-blocker, carbonic anhydrase inhibitor, or sympathomimetic eyedrop
123
Q

Vitreous haemorrhage

Vitreous haemorrhage is bleeding into the vitreous humour. It is one of the most common causes of sudden painless loss of vision.

A

Common causes: proliferative diabetic retinopathy (over 50%)
Patients typically present with an acute or subacute onset of:

  • painless visual loss or haze (commonest)
  • red hue in the vision
  • floaters or shadows/dark spots in the vision
  • dilated fundoscopy: may show haemorrhage in the vitreous cavity
124
Q

Retinal Detachment

reversible cause of visual loss. must be treated before macula damage

Retinal detachment occurs when the neurosensory tissue that lines the back of the eye comes away from its underlying pigment epithelium.

A

RF: DM, Myopia

  • sudden onset, painless and progressive visual field loss, described as a curtain or shadow progressing to the centre of the visual field from the periphery

if the macula is involved, central visual acuity and visual outcomes become much worse

  • any patients with new onset flashes and floaters should be referred urgently (<24 hours) to an ophthalmologist for assessment with a slit lamp and indirect ophthalmoscopy for pigment cells and vitreous haemorrhage
125
Q

Central Retinal artery occlusion

‘cherry red’ spot on a pale retina

A
  • a relatively rare cause of sudden unilateral visual loss. It is due to thromboembolism (from atherosclerosis) or arteritis (e.g. temporal arteritis)
  • any underlying conditions should be identified and treated (e.g. intravenous steroids for temporal arteritis)
    if a patient presents acutely then Intraarterial thrombolysis may be attempted but currently, trials show mixed result
126
Q

Central retinal vein occlusion

A
  • sudden, painless reduction or loss of visual acuity, usually unilaterally
  • severe retinal haemorrhages - ‘stormy sunset’
  • managment
    macular oedema - intravitreal anti-vascular endothelial growth factor (VEGF) agents
    retinal neovascularization - laser photocoagulation
127
Q

Optic Neuritis

MS, Diabetes, Syphillis

A
  • unilateral decrease in visual acuity over hours or days
  • poor discrimination of colours, ‘red desaturation’
  • pain worse on eye movement
  • relative afferent pupillary defect
  • central scotoma

Management
* high-dose steroids
* recovery usually takes 4-6 weeks

128
Q

Cataracts

more common in women

A

where the lens of the eye gradually opacifies i.e. becomes cloudy. This cloudiness makes it more difficult for light to reach the back of the eye (retina), thus causing reduced/blurred vision.
- Surgery required

129
Q

Syringomyelia

Causes:a Chiari malformation, trauma, tumours, idiopathic

Syringomyelia (‘syrinx’ for short) describes a collection of cerebrospinal fluid within the spinal cord.

A

a ‘cape-like’ (neck, shoulders and arms)

  • loss of sensation to temperature but the preservation of light touch, proprioception and vibration
  • classic examples are of patients who accidentally burn their hands without realising
  • this is due to the crossing spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected
  • Horner’s syndrome due to compression of the sympathetic chain, but this is rare
  • scoliosis will occur over a matter of years if the syrinx is not treated
  • Spastic weakness
  • Full spine and Brain MRI

Treatment will be directed at treating the cause of the syrinx. In patients with a persistent or symptomatic syrinx, a shunt into the syrinx can be placed.

130
Q

Idiopathic intracranial hypertension

A
131
Q

Multisystem Atrophy

A
132
Q

Valsalva Headaches

A

3a Notes AC (20 decks)

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