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Medicine > Neurology > Flashcards

Neurology Flashcards

1
Q

UMN lesion features

A 
Weakness
Spasticity (increased tone, clasp knife rigidity)
Hyperreflexia
Positive babinski (upgoing plantars)
Clonus
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2
Q

LMN lesion feature

A 
Weakness
Wasting
Fasciculation
Hypotonia/flaccid paralysis
Hyporeflexia
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3
Q

Sensory deficits and their location in the cord

A

Pain and temperature - small fibres in peripheral nerves and anterolateral spinothalamic tract in the cord and brainstem

Proprioception and vibration - large fibres in peripheral nerves and dorsal column medial lemniscus of the cord

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4
Q

Features of lesion in internal capsule and corticospinal trct

A

contralateral hemiparesis (UMN), generalised contralateral sensory loss

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5
Q

Brainstem lesion features

A

Ipsilateral cranial nerve palsy and contralateral hemiplegia

Lateral brain stem lesion - dissociated and crossed sensory loss with loss of pain and temperature on the side of the face ipsilateral to the lesion, and contralateral arm and leg sensory loss

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6
Q

Cord lesion features

A

Paralysis below the level of the lesion. LMN signs at the level of the lesion and UMN signs below the lesion. A sensory level is the hallmark.

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7
Q

Peripheral neuropathy features

A

Distal weakness, sensory loss is typically worse distally

Involvement of a single nerve may occur with trauma/entrapment
Sensory loss with mononeuropathies will follow dermatomal territories

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8
Q

What do the internal carotid arteries supply

A

Anterior two-thirds of the cerebral hemispheres and the basal ganglia (via the lenticulostriate arteries)

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9
Q

Which arteries make up the circle of willis?

A

Internal carotids (anteriorly), basilar artery (posteriorly, formed by joining the vertebral arteries), anterior cerebral arteries, anterior communicating arteries, posterior communicating arteries, posterior cerebral arteries

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10
Q

Headache red flags

A
  • Immunocompromised
  • <20 with malignancy
  • Vomiting without an obvious cause
  • Worsening headache + fever
  • Sudden onset headache reaching max intensity within 5 mins (thunderclap)
  • New onset neuro deficit
  • New onset cognitive dysfunction
  • Change in personality
  • Impaired consciousness
  • Recent head trauma
  • Headache triggered by cough/sneeze/ exercise
  • Orthostatic headache
  • Symptoms suggestive of giant cell arteritis or acute narrow-angle glaucoma
  • Substantial change in the characteristics of their headache
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11
Q

Differentials for rapid onset headache

A 
SAH
Meningitis
Encephalitis
Post-coital headache
Head trauma
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12
Q

Differentials for subacute/gradual onset headache

A 
Venous sinus thrombosis
Sinusitis
Giant cell arteritis
Tropical illness (malaria)
Intracranial hypotension
Idiopathic intracranial hypertension
Glaucoma
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13
Q

Differentials for chronic headache

A 
Migraine
Tension headache
Medication overuse headache
Cluster headache
Visual defects
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14
Q

Cluster headache risk factors

A

Male
Smokers
Alcohol may trigger an attack

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15
Q

Cluster headache features

A

Pain typically once/twice a day, lasting 15min-2hrs
The clusters typically last 4-12 weeks
Intense sharp stabbing pain around one eye (always affects same eye in one cluster)
Patient is restless and agitated during attack
Accompanied by redness, lacrimation and lid swelling
Nasal stuffiness
Miosis and ptosis in some

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16
Q

Management of cluster headache

A

Acute: 100% oxygen, subcut triptan

Prophylaxis: verapamil

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17
Q

Migraine features

A

Severe, unilateral throbbing headache
Nausea, photophobia, phonophobia
May last up to 72 hours

May be precipitated by an aura: visual, progressive, lasts 5-60mins, transient hemianopic disturbance or a spread of scintillating scotoma

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18
Q

Common triggers for a migraine

A

Tiredness, stress, alcohol, COCP, hunger, dehydration, cheese, chocolate, red wines, citrus fruits, menstruation, bright lights

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19
Q

Migraine diagnostic criteria

A

At least 5 attacks fulfilling the following criteria:

= Headache attacks lasting 4-72 hours
= Headache has at least two of the following: unilateral, pulsating, moderate/severe pain, aggravated by physical activity
= During headache at least one of: nausea and/or vomiting, photophobia and phonophobia
= Not attributed to another disorder

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20
Q

Acute treatment of migraines

A

First line: combination therapy with an oral triptan and an NSAID/paracetamol
-Consider nasal triptan rather than oral in children aged 12-17

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21
Q

Migraine prophylaxis

A

Given to patients who experience 2+ attacks/month

First line: Topiramate or propranolol (patient preference)
Propranolol for women of child bearing age

Second line: up to 10 sessions of acupuncture

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22
Q

Management of migraines during pregnancy

A

1g paracetamol is first line
NSAIDs can be used second-line in first and second trimester

Avoid aspirin and opioids

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23
Q

Absence seizures

  • Epidemiology
  • Features
  • EEG
  • Management
A

Generalised epilepsy, most common in children (4-8y, girls>boys)

Features: lasts a few seconds with quick recovery, may be provoked by hyperventilation or stress, child is usually unaware of the seizure, may occur many times a day

EEG: bilateral, symmetrical 3Hz spike and wave pattern

Management: sodium valproate and ethosuximide are first line

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24
Q

Carbamazepine

  • uses
  • MoA
  • adverse effects
A

First-line for partial seizures
Also used in trigeminal neuralgia and bipolar disorder

MoA: binds to sodium channels increasing their refractory period

Adverse effects: P450 inducer, SIADH (hyponatraemia), dizziness, ataxia, drowsiness, headache, diplopia, Steven-Johnson, leucopenia, agranulocytosis

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25
Q

Differentials for non-epileptic recurrent seizures

A

Febrile convulsions
Alcohol withdrawal seizures
Psychogenic non-epileptic seizures

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26
Q

Alcohol withdrawal seizures

-who, when, how to reduce risk

A

Occurs in patients with history of alcohol excess who suddenly stop drinking
Typically occurs 36 hours after stopping drinking
Patients are often given benzodiazepines (chlordiazepoxide) following alcohol cessation to reduce risk

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27
Q

What are focal/partial seizures and how are they classified

A

Starts in a specific area, on one side of the brain
Level of awareness varies (focal aware, or focal impaired awareness)
Can be further classified as being motor (eg. jacksonian march), non-motor (eg. deja vu) or having other features (eg. aura)

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28
Q

Generalised seizures

  • what are they
  • consciousness
  • subclassification
  • specific types
A

Both sides of the brain are involved at onset
Consciousness lost immediately
Can be subdivided into motor (eg. tonic-clonic) and non-motor (eg. absence)

Specific types: tonic-clonic, tonic, clonic, typical absence, myoclonic, atonic

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29
Q

What are focal to bilateral seizures?

A

Starts on one side of the brain in a specific area before spreading to both lobes

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30
Q

Features of generalised seizures

A

May have an aura beforehand
During seizure: tongue biting, urine incontinence
Postictal phase: drowsiness, tiredness for about 15mins

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31
Q

Investigations following a seizure

A

EEG

MRI

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32
Q

Antiepileptics

A

Antiepileptics are started following a second epileptic seizure

Sodium valproate is usually first line for generalised seizures
Carbamazepine is generally first line for focal seizures
Lamotrigine can also be used first line for focal seizures, and is second line for most generalised seizures. Suitable alternative to valproate in women of child bearing age

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33
Q

DVLA and seizures

A

No driving for 6m following a seizure

Must be seizure free for 12m if patient has established epilepsy

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34
Q

Sodium valproate

  • Uses
  • MoA
  • Adverse effects
A
  • First line for generalised seizures
  • Increases GABA activity
  • SE: teratogenic, weight gain, P450 inhibitor, alopecia, ataxia, tremor, hepatitis, pancreatitis, thrombocytopenia
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35
Q

Lamotrigine

  • Uses
  • MoA
  • Adverse effects
A
  • Second-line for a variety of generalised and partial seizures
  • MoA: sodium channel blocker
  • SE: Stevens-Johnson syndrome
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36
Q

Phenytoin

  • Uses
  • MoA
  • Adverse effects
A
  • Used in status epilepticus
  • MoA: binds to sodium channels, increasing their refractory period
  • SE: P450 inducer, dizziness, ataxia, gingival hyperplasia, drowsiness, coarsening of facial features, hirsutism, megaloblastic anaemia, peripheral neuropathy, osteomalacia, lymphadenopathy
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37
Q

Managing a patient during a seizure (not status epilepticus)

A

Protect form injury - cushion the head, remove glasses, remove harmful objects nearby
Do not restrain or put anything in the mouth

Most seizures terminate spontaneously
If a seizure has not terminated after 5-10 mins then patient should be given a benzodiazepine (IV lorazepam, buccal midazolam, PR diazepam). Patients should have these with them in the community, and family members should be taught how to administer them.
If patient continues to fit despite these measures = status epilepticus

When seizure stops, check airways and put in recovery position, and observe until they have recovered fully

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38
Q

West’s syndrome

  • what is it
  • what happens
  • EEG
  • Prognosis
  • Management
A

Infantile spasms beginning at 4-6m of life (M>F)
Flexion of head, trunk and limbs -> extension of arms (Salaam attack), lasts 1-2secs, repeats up to 50 times
Progressive mental handicap
EEG: hypsarrhythmia

Usually secondary to neurological abnormality
Poor prognosis

Give vigabatrin/ steroids

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39
Q

Features of focal epileptic seizures based on location

  • temporal
  • frontal
  • parietal
  • occipital
A
  • Temporal (HEAD): hallucinations, epigastric rising/emotional, automatisms (lip smacking, grabbing, plucking), deja vu/dysphasia post-ictal
  • Frontal: head/leg movements, posturing, post-ictal weakness, jacksonian march
  • Parietal: paraesthesia
  • Occipital: floaters/ flashes
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40
Q

Features favouring psychogenic non-epileptic seizures over a true epileptic seizure

A

Pseudoseizure: pelvic thrusting, family member with epilepsy, much more common in females, crying after seizure, dont occur when alone, gradual onset

True epileptic seizure: tongue biting, raised serum prolactin

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41
Q

Management of status epilepticus in the hospital

A

Secure airway + 100% oxygen
Assess cardioresp function
Check blood glucose, FBC, calcium, U+E, LFT, +/- tox screen, anticonvulsant levels
Secure IV access

Anaesthetist should be at the bedside if patient has been seizing for 20min

IV bolus of lorazepam 4mg
Repeat if no response after 10-20min

Thiamine 250mg IV over 30 min if alcoholism or malnutrition suspected

Give glucose 50ml 50% IV, unless glucose known to be normal

Treat acidosis if severe (contact ICU)

Correct hypotension with fluids

IV phenytoin infusion if seizure continues, monitor ECG and BP

If seizure continues after 60-90min, ventilation and propofol infusion for rapid sequence induction is needed (ITU)

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42
Q

Investigations during status epilepticus

A

Bedside glucose
Once treatment has started do the following: lab glucose, ABG, U+E, calcium, FBC, ECG
Consider anticonvulsant levels, tox screen, LP, culture blood and urine, EEG, CT, carbon monoxide level
Pulse oximetry, cardiac monitor

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43
Q

Tension type headache characteristic features

A

Tight band around the head or a pressure sensation
Symptoms are bilateral (migraine = unilateral)
Tends to be a lower intensity than a migraine
Not associated with aura, N+V or aggravated by activity
May be related to stress
May co-exist with migraine

Chronic tension type headache = tension headache occurring on 15+ days per month

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44
Q

Management of tension type headaches

A

Acute: aspirin, paracetamol or NSAID

Prophylaxis: up to 10 sessions of acupuncture over 5-8 weeks

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45
Q

Definition of a transient ischaemic attack

A

A transient neurological dysfunction secondary to ischaemia without infarction.
Lasts less than 24 hours.

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46
Q

What is a crescendo TIA?

A

TIAs often precede a full stroke.

A crescendo TIA is where there are two or more TIAs within a week. This carries a high risk of progressing to a stroke

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47
Q

When to suspect a stroke?

A

SUDDEN onset of neurological symptoms = vascular cause

Typically asymmetrical: sudden weakness of limbs, sudden facial weakness, sudden dysphasia, sudden visual or sensory loss

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48
Q

Risk factors for a stroke

A 
Cardiovascular disease
Previous stroke or TIA
AF
Carotid artery disease
Hypertension
Diabetes
Smoking
Vasculitis
Thrombophilia
Combined oral contraceptive pill
Anticoagulation (-haemorrhagic)
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49
Q

Tool used in the community for recognising a stroke

A 
FAST
Face
Arms
Speech
Time to call 999
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50
Q

Tool used in A+E for recognising a stroke

A

ROSIER
‘Recognition of stroke in emergency room’

Exclude hyperglycaemia first, then assess the following:
LOC or syncope = -1
Seizure activity = -1
Acute onset of asymmetrical face weakness = +1
Acute onset of asymmetrical arm weakness = +1
Acute onset of asymmetrical leg weakness = +1
Acute onset of speech disturbance = +1
Acute onset of visual field defect = +1

Stroke is likely if the patient scores anything above 0

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51
Q

Scoring tool used for patients with TIA

A

ABCD2
Used for assessing patients with a suspected TIA to estimate their risk of subsequently having a stroke. A higher score suggests a higher risk of stroke within the following 48 hours.
NICE no longer recommend using this.

Age >60 (1)
Blood pressure >140/90 (1)
Clinical features: unilateral weakness (2), dysphasia without weakness (1)
Duration: >60min (2), 10-60min (1), <10min (0)
Diabetes (1)

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52
Q

Classification of strokes

A

Oxford stroke classification

The following criteria is assessed:

  1. Unilateral hemiparesis and/or hemisensory loss of the face, arm and leg
  2. Homonymous hemianopia
  3. Higher cognitive dysfunction (eg. dysphasia)

Total anterior circulation infarct (TACI): involves middle and anterior cerebral arteries. All 3 of above criteria present.

PACI: involves smaller arteries of anterior circulation. 2 of above criteria present.

POCI: involves vertebrobasilar arteries. Presents with 1 of the following:

  1. Cerebellar or brainstem syndromes
  2. LOC
  3. Isolated homonymous hemianopia

Lacunar: involves perforating arteries around the internal capsule, thalamus and basal ganglia.
Presents with 1 of the following:
1. unilateral weakness and/or sensory deficit of face and arm, arm and leg, or all three
2. Pure sensory stroke
3. Ataxic hemiparesis

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53
Q

Management of ischaemic stroke

A

Immediate CT brain within 1hr to exclude haemorrhage.
If thrombectomy might be indicated, perform CT contract angiography after the initial non-enhanced CT

Aspirin 300mg stat (after CT) and continue for 2 weeks, then switch to lifelong clopidogrel 75mg OD

Thrombolysis with alteplase if CT excludes haemorrhage
Thrombectomy also considered in some patients

Keep NBM until swallow screen is done

Maintain BMs between 4-11

Start on statin if cholesterol >3.5 (dealy until after 48 hours due to risk of haemorrhagic transformation)

If patient has AF: dont start anticoag until 14 days have passed

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54
Q

Management of suspected TIA

A

Stat aspirin 300mg and continue for 14 days then switch to clopidogrel 75mg

Carotid endarterectomy required within 2 weeks if carotid artery is 70-99% stenosed and operative risk is acceptable

Stop driving for 1 month

If patient has had >1 TIA (crescendo) or has suspected cardioembolic source or severe carotid stenosis: discuss admission to stroke specialist

If patient has had suspected TIA in last 7 days: arrange urgent assessment within 24hrs by stroke specialist (TIA clinic)

If patient has had suspected TIA more than a week ago: refer for specialist assessment ASAP within 7 days

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55
Q

Management of haemorrhagic stroke

A

CT confirms haemorrhage
Neurosurgical consultation should be considered
Most patients arent suitable for surgery, management si therefore supportive

Stop anticoags and antithrombotics
Reverse any anticoagulation

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56
Q

Criteria for thrombolysis
Absolute contraindications
Relative contraindications

A

Must be administered within 4.5 hours of onset of stroke symptoms

Haemorrhage must be definitively excluded

Absolute contraindications: previous intracranial haemorrhage, seizure at onset of stroke, intracranial neoplasm, suspected SAH, stroke or traumatic brain injury in preceding 3m, LP in preceding 7 days, GI haemorrhage in preceding 3 weeks, active bleeding, pregnancy, oesophageal varices, uncontrolled HTN >200/120

Relative contraindications: concurrent anticoag, haemorrhage diathesis, active diabetic haemorrhagic retinopathy, suspected intracardiac thrombus, major surgery/trauma in preceding 2 weeks

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57
Q

Criteria for mechanical thrombectomy

A

Pre-stroke function status of less than 3 on modified Rankin scale
Score of >5 on NIHSS

Offer thrombectomy as soon as possible and within 6 hours of symptom onset, together with IV thrombolysis (within 4.5hours), to people who have: acute ischaemic stroke, and confirmed occlusion fo proximal anterior circulation demonstrated by CT angiography (or MR angiography)

Offer thrombectomy as soon as possible to people who were healthy/well between 6-24 hours previously: who have acute ischaemic stroke and confirmed occlusion of proximal anterior circulation demonstrated by CTA, and if there is the potential to salvage brain tissue as shown on CT perfusion or diffusion-weighted MRI

Consider thrombectomy with IV thrombolysis ASAP for people last known to be well up to 24 hours previously: who have acute ischaemic stroke and confirmed occlusion of proximal posterior circulation demonstrated by CTA, and if there is potential to salvage brain tissue as shown on CT perfusion or diffusion-weighted MRI

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58
Q

Secondary prevention of ischaemic stroke

A

Clopidogrel 75mg OD lifelong

Carotid doppler US +/- CT/MRI angiography -> Carotid endarterectomy for patients who have carotid stenosis >70% (ECST criteria)

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59
Q

Barthel’s index of activities of daily living

A

Assesses 10 ADLs: bowels, bladder, grooming, toilet use, feeding, transfer, mobility, dressing, stairs, bath/shower

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60
Q

Stroke mimics

A

Group 1 – readily identifiable on brain imaging

  • Subdural haematomas
  • Tumours
  • Brain abscesses
  • MS – may present acutely with focal neurology

Group 2 – identifiable after general assessment based on clinical knowledge

  • Syncope syndrome
  • BPPV
  • Vestibular neuritis
  • Transient global amnesia

Group 3 – distinguishable after specialist stroke assessment and brain imaging

  • Migraine with aura
  • Focal seizures
  • Functional syndrome
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61
Q

Stroke features by anatomy

  • anterior cerebral artery
  • middle cerebral artery
  • posterior cerebral artery
  • Ophthalmic artery
  • Basilar artery
A
  • Anterior cerebral artery: contralateral hemiparesis and sensory loss (lower limb > upper limb because of homunculus)
  • Middle cerebral artery: contralateral hemiparesis and sensory loss (upper limb > lower limb because of homunculus), contralateral homonymous hemianopia, aphasia
  • Posterior cerebral artery: contralateral homonymous hemianopia with macular sparing, visual agnosia
  • Ophthalmic artery: amaurosis fugax
  • Basilar artery: locked in syndrome
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62
Q

Stroke syndromes:

  • Webers syndrome
  • Wallenberg syndrome
  • Lateral pontine syndrome
A
  • Webers: branches of posterior cerebral artery that supply midbrain. Ipsilateral CNIII palsy, contralateral weakness of upper and lower limbs
  • Wallenbergs: lateral medullary syndrome. Posterior inferior cerebellar artery. Ipsilateral facial pain and temp loss, contralateral limb/torso pain and temp loss, ataxia, nystagmus
  • Lateral pontine: anterior inferior cerebellar artery. Symptoms similar to wallenbergs but ipsilateral facial paralysis and deafness
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63
Q

MDT input for stroke treatment

A 
Doctors
Nurses
SALT
Nutrition and dietetics
PT
OT
Social services
Optometry and ophthalmology
Psychology
Orthotics
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64
Q

Non-contrast CT features of early ischaemia

A

Increased density of the relevant blood vessel due to the presence of clotted blood

Loss of grey-white matter differentiation, hypodensity of cortical tissue

Obscuration of the lentiform nucleus (seen in MCA occlusion)

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65
Q

National Institute of Health Stroke Scale

A

A tool used to assess the severity of a stroke.

1) Level of consciousness:
a) Level of consciousness (level of alertness) (0-3)
b. LOC questions (verbal) (0-2)
c. LOC commands (visual and motor) (0-2)
2) Best gaze (0-2)
3) Visual fields (0-3)
4) Facial palsy (0-3)
5) Arm motor (0-4)
6) Leg motor (0-4)
7) Limb ataxia (0-2)
8) Sensory (0-2)
9) Best language (0-3)
10) Dysarthria (0-2)
11) Extinction and inattention, formerly called neglect (0-2)

0 = no stroke symptoms
1-4 = minor stroke
 5-15 = moderate stroke
16-20 = moderate/ severe
21-42 = severe stroke
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66
Q

Complications of thrombolysis

A

Extracerebral haemorrhage-> thread pulse, ↓ BP, melaena, distended abdo
New headache
Acute hypertension
Nausea and vomiting

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67
Q

Complications of stroke

A

Recurrent stroke and extension of stroke

Raised intracranial pressure – haematoma expansion, malignant oedema, haemorrhagic transformation, hydrocephalus

Infection – chest infections due to aspiration, UTIs due to incomplete bladder emptying from either constipation or bed bound position

Complications of immobility - VTE, constipation, bed sores

Mood and cognitive dysfunction (this can affect compliance and rehabilitation)

Post stroke pain and fatigue - spasticity, joint dislocation or central/neuropathic pain, poor sleep, medications, inherent result of brain cell damage

Spasticity, contractures and secondary epilepsy

Premature death – usually related to post-stroke complications rather than the stroke itself

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68
Q

Modified Rankin Scale

A

Scale used for measuring the degree of disability following a stroke, determining the need for PT/OT therapy and the degree of care required

0 – no symptoms
1 – no significant disability. Able to carry out usually activities, despite some symptoms
2 – Slight disability. Able to look after own affairs without assistance, but unable to carry out all previous activities
3 – moderate disability. Requires some help but able to walk unassisted
4 – moderately severe disability. Unable to attend to own bodily needs without assistance, and unable to walk unassisted
5 – severe disability. Requires constant nursing care and attention, bedridden, incontinent
6 - dead

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69
Q

Causes of SAH

A

Traumatic (most common)

Spontaneous - 
Intracranial aneurysm (berry aneurysms)
Arteriovenous malformation
Pituitary apoplexy
Arterial dissection
Mycotic aneurysms
Perimesencephalic
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70
Q

Clinical features of SAH

A 
Sudden onset thunderclap headache, like a baseball bat to the occipital region
N+V
Meningism (photophobia, neck stiffness)
Coma
Seizures
Sudden death
ECG changes may include ST elevation
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71
Q

Diagnosing SAH

A

CT head: acute blood (hyperdense/bright on CT). false negative in 7% of cases.

LP used to confirm SAH if CT is negative but there is still clinical suspicion. Performed at least 12 hours following onset of symptoms to allow for development of xanthochromia (LP findings with SAH = xanthochromia + normal or raised opening pressure)

After spontaneous SAH is confirmed, investigations for a cause:
CT intracranial angiogram (aneurysms, AVM, etc)
Digital subtraction angiogram

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72
Q

Management of SAH

  • aneurysmal SAH management
  • management of vasospasms
  • management of hydrocephalus
A

Spontaneous SAH should be managed by treating the underlying cause.

SAH due to intracranial aneurysm: usually treated with a coil by interventional neuroradiologists, but some need a craniotomy and clipping by a neurosurgeon. Intervention should be done within 24hrs due to risk of rebleeding. Until the aneurysm is treated, patient should be kept of strict bed rest with well-controlled BP and should avoid straining.

Vasospasm is prevented using a 21 day course of nimodipine (CCB), and is treated with hypovolaemia induced-hypotension and haemodilution

Hydrocephalus is temporarily treated with an external ventricular drain (CSF diverted into a bag at the bedside) or if required, a long term ventriculo-peritoneal shunt

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73
Q

Complications of aneurysmal SAH

A 
Re-bleeding
Vasospasm (typically 7-14 days later)
Hyponatraemia (SIADH)
Seizures
Hydrocephalus
Death
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74
Q

Extradural haematoma

  • what is it
  • cause
  • presentation
  • CT
  • Mx
A

Collection of blood between the skull and the dura

Caused by low impact trauma

  • > LOC, a lucid interval, and then a rapid decline in consciousness
  • > Mass effect on the brain will cause uncal herniation and a fixed dilated pupil due to CNIII compression

CT: hyperdense (bright) biconvex collection around the surface of the brain

Definitive mx: craniotomy and evacuation of the haematoma

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75
Q

Acute subdural haematoma

  • what is it
  • cause
  • presentation
  • CT
  • Mx
A

Fresh collection of blood under the layer of the dura

Commonly caused by trauma but can be caused by vascular lesions
Typically caused by high speed injuries or acceleration-deceleration injuries

Varies in clinical picture from an asymptomatic patient to a severely comatose patient

CT: hyperdense (bright) crescenteric collection, not limited by suture lines, +/- midline shift

Definitive Mx: decompressive craniotomy

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76
Q 
Chronic subdural haematoma
-what is it
-who does it occur in
-presentation
-CT
Mx
A

Old collection of blood that is under the layer of the dura

More common in elderly, alcoholics, people on anticoag, or in infants due to fragility of bridging veins

Typically presents several weeks after a mild head injury with progressive confusion, LOC, weakness, or higher cortical dysfunction

CT: hypodense (dark) crescenteric collection around the surface of the brain that is not limited by suture lines

Mx: if symptomatic, definitive mx is burr hole drainage

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77
Q

Intracerebral haematoma

  • what is it
  • risk factors
  • presentation
  • CT
  • Mx
A

Collection of blood within the substance of the brain

Risk factors: HTN, aneurysm, AV malformation, cerebral amyloid angiopathy, brain tumour, infarct

Typically presents similarly to an ischaemic stroke, or with a decrease in consciousness

CT: hyperdensity (bright) within the substance of the brain

Mx: conservative under the care of the stroke physicians, but large clots in patients with impaired consciousness may warrant surgical evacuation

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78
Q

Glasgow coma scale

A

Eyes (4): spontaneous, speech, pain, none

Verbal (5): orientated, confused conversation, inappropriate words, incomprehensible sounds, none

Motor (6): obeys commands, localises pain, normal flexion, abnormal flexion, extension, none

If GCS 8, ventilate.

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79
Q

Risk factors and causes of delirium

A 
Age >65
Background of dementia
Significant injury (eg. hip fracture)
Frailty or multimorbidity
Polypharmacy

Infection (esp UTI)
Metabolic (hypercalcaemia, hypoglycaemia, hyperglycaemia, dehydration)
Change of environment
Any significant cardiac, resp, neuro, or endocrine condition
Severe pain
Alcohol withdrawal
Constipation

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80
Q

Factors favouring delirium over dementia

A

Impairment of consciousness
Fluctuation of symptoms (worse at night, periods of normality)
Abnormal perception (illusions and hallucinations)
Agitation
Fear
Delusions

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81
Q

Types of delirium

A

Hyperactive: restlessness, mood lability, agitation, aggression

Hypoactive: slow and withdrawn

Mixed

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82
Q

Investigations for delirium

A

Look for the cause
FBC, U+E, LFT, blood glucose, ABG, septic screen (urine dip, CXR, cultures)

Consider ECG, malaria films, LP, EEG, CT

83
Q

Management of delirium

A 
Identify and treat underlying cause
Reorientate patient
Encourage visits from friends and family
Monitor fluid balance and encourage oral intake
Mobilise and encourage physical activity
Practise sleep hygiene
Avoid or remove catheters, IV cannulae, monitoring leads and other devices
Watch out for infection and distress
Review medication

Only use sedation if the patient is at risk to their own/other patient’s safety. Consider haloperidol.

84
Q

Management of new dementia

A

Blood screen to exclude reversible causes: FBC, U+E, LFT, calcium, glucose, TFTs, vit B12 and folate

Neuroimaging to exclude other reversible conditions

Referral to an old age psychiatrist (memory clinics)

85
Q

Causes of dementia

A

Alzheimers disease
Cerebrovascular disease
Lewy body dementia

Picks disease (frontotemporal)
Huntingtons
CJD
HIV

Important potentially treatable:
Hypothyroidism
Addisons
B12/folate/thiamine deficiency
Syphilis
Brain tumour
Normal pressure hydrocephalus
Subdural haematoma
Depression
Chronic drug use
86
Q

Pathological changes of Alzheimers disease

  • macroscopic
  • microscopic
  • biochemical
A
  • Macroscopic: widespread cerebral atrophy, particularly cortex atrophy and hippocampus atrophy
  • microscopic: cortical plaques due to deposition of type A-beta-amyloid protein and intraneuronal neurofibillary tangles caused by abnormal aggregation of the tau protein
  • biochemical: ACh deficit from damage to an ascending forebrain projection
87
Q

Management of Alzheimers disease

A

Non-pharmacological: activities to promote wellbeing, group cognitive stimulation therapy, group reminiscence therapy and cognitive rehabilitation

Pharmacological:
Mild-mod: AChesterase inhibitors (donepezil, galantamine, rivastigmine)
Moderate-severe: NMDA antagonist (memantine)

88
Q

Clinical features of Alzheimers disease

A

Memory loss
Impaired visual-spatial skill and verbal skill
Behavioural changes
Agnosia (unable to recognise self in mirror)
Lack of insight
Eventually patient becomes sedentary, taking little interest in anything

89
Q

Lewy Body dementia

  • pathological features
  • associated disease
  • features
  • diagnosis
  • management
A

Alpha-synuclein cytoplasmic inclusions (Lewy bodies) in the substantia nigra, paralimbic and neocortical areas
Associated with Parkinsons disease

Features:
Progressive cognitive impairments in attention and executive function rather than just memory loss (unlike alzheimers), cognition may be fluctuating
Parkinsonism
Visual hallucinations

Diagnosis: clinical
Single-photon emission computed tomography (SPECT) -DaTscan

Management: Achesterase inhibitors (donepezil), NMDA antagonists (memantine)

Avoid neuroleptics and the patient may develop irreversible parkinsonism

90
Q

Pick’s disease

  • what is it
  • features
  • macroscopic changes
  • microscopic changes
A

frontotemporal dementia

Features: personality change, impaired social conduct, hyperorality, disinhibition, increased appetite, perseveration behaviours

Macroscopic changes: atrophy of the frontal and temporal lobes

Microscopic: pick bodies (aggregations of tau protein), neurofibrillary tangles, gliosis, senile plaques

91
Q

Parkinsons disease features

A

Triad:

  1. Resting tremor (pill rolling)
  2. Hypertonia (rigidity + tremor gives cogwheel rigidity)
  3. Bradykinesia (slow to initiate)

Actions slow and decrease in amplitude with repetition, eg. micrographia

Festinant gait (shuffling, pitched forward, reduced arm swing)

Signs tend to be worse on one side

Expressionless face
REM sleep behaviour disorder
Fatigue
Postural hypotension
Depression
92
Q

Diagnosis of parkinsons disease

A

Clinical diagnosis, based on symptoms and examination
The diagnosis should be made by a specialist (GP should refer to a neurology clinic)

UK Parkinsons Disease Society brain bank clinical diagnostic criteria

93
Q

Parkinsons tremor vs benign essential tremor

A

Parkinsons: asymmetrical, 4-6 hertz, worse at rest, improves with intentional movement, other parkinsons features present, no change with alcohol

Benign essential tremor: symmetrical, 5-8Hz, improves at rest, worse with intentional movement, no other parkinsons features, improves with alcohol

94
Q

Management of Parkinsons disease

A

First-line if motor symptoms are affecting a patient’s QoL: levodopa and decarboxylase inhibitor (=co-careldopa)

First line if motor symptoms are not affecting QoL: non-ergot derived dopamine agonist, co-careldopa, or MAO-B inhibitor

If patient is on co-careldopa and has symptoms despite max treatment or starts developing dyskinesia, then add a dopamine agonist, MAO-B inhibitor or COMT inhibitor as an adjunct

Parkinson’s patients must always have their medication on time due to the risk of acute akinesia or neuroleptic malignancy syndrome if medication is not taken/absorbed

95
Q

Management of postural hypotension in parkinsons patients

A

Medication review first
If symptoms persist then midodrine can be considered (increases peripheral arterial resistance by acting on alpha adrenergic receptors)

96
Q

Levodopa

  • which medication should it be combined with and why
  • complications
  • side effects
A

Combined with decarboxylase inhibitor (=co-careldopa) to prevent peripheral metabolism of levodopa into dopamine

Reduced effectiveness with time (approx 2 years)

SEs: dyskinesia, on-off effect, dry mouth, anorexia, palpitations, postural hypotension, psychosis, drowsiness

Don’t stop medication suddenly. Dopamine agonist patch should be given if drugs cant be taken orally, to prevent acute dystonia

97
Q

Dopamine agonists

  • ergot derived dopamine agonist side effects and monitoring requirements
  • side effects of dopamine agonists
A

Ergot-Derived: bromocriptine, cabergoline. Associated with pulmonary, retroperitoneal and cardiac fibrosis. Echo, ESR, creatinine and CXR should be done before treatment and patients should be closely monitored

Non-ergot derive (ropinirole)

Dopamine agonists may cause impulse control disorders and excessive daytime somnolence

More likely to cause hallucinations than levodopa. Nasal congestion and postural hypotension also seen in some patients

98
Q

Monoamine-oxidase B inhibitors

-MoA

A

Eg. Selegiline
Inhibits breakdown of dopamine secreted by dopaminergic neurones

Not useful in later disease when dopaminergic neurones stop secreting dopamine

SEs: postural hypotension, AF

99
Q

Amantadine

A

Mechanism not fully understood, but may increase dopamine release and inhibit its uptake at dopaminergic synapses

SEs: ataxia, slurred speech, confusion, dizziness, livedo reticularis

100
Q

Sleep disorders and parkinsons

+management

A

Parkinsons patients may experience restless leg syndrome and REM sleep behaviour disorder

Consider clonazepam or melatonin to treat this

101
Q

Non-pharmacological management of parkinsons disease

A

Physiotherapy referral
Occupational therapy
SALT for patients who are experiencing problems with communication, swallowing or saliva
Dietitian input

102
Q

Parkinson’s-plus syndromes

A

Multiple System Atrophy: early autonomic features (impotence, incontinence), postural hypotension, cerebellar and pyramidal signs, rigidity > tremor

Lewy Body dementia

Progressive supranuclear palsy: early postural instability, vertical gaze palsy, falls, rigidity of trunk > limbs, symmetrical symptoms, speech and swallow problems, little tremor

Corticobasal degeneration: akinetic rigidity involving one limb, cortical sensory loss, apraxia (alien limb phenomenon)

103
Q

Secondary causes of parkinsonism

A

Vascular parkinsonism: diabetic/hypertensive patients with postural instability and falls
Drug-induced (antipsychotics, metoclopramide)
Wilsons disease
Post-encephalitis
Dementia pugilistica (secondary to chronic head trauma)
Toxins (carbon monoxide)
Neurosyphilis

104
Q

Differential diagnoses of a tremor

A 
Parkinsons disease
Benign essential tremor
Anxiety
CO2 retention
Cerebellar disease
Drug withdrawal
MS
Huntingtons Chorea
Hyperthyroidism
Fever
Medications (eg. antipsychotics)
105
Q

Neuroleptic malignant syndrome

  • cause
  • pathophysiology
  • features
  • ix
  • mx
A

Rare but dangerous condition seen in patients who take anti-dopaminergic antipsychotics or parkinsons patients who stop their drugs suddenly

Pathophysiology: dopamine blockade triggers a massive release of glutamate and subsequent neurotoxicity and muscle damage

Occurs within hours to days of starting an antipsychotic or stopping parkinsons meds

-> pyrexia, muscle rigidity, autonomic lability (HTN, tachycardia, tachypnoea), agitated delirium with confusion

Ix: raised creatine kinase, AKI, leukocytosis

Mx: stop antipsychotic, transfer to a medical ward or ICU, IV fluids prevent renal failure, dantrolene may be required in selective cases, bromocriptine or other dopamine agonists may be needed

106
Q

Multiple sclerosis

  • what is it/ pathophysiology
  • epidemiology
  • subtypes
A

Chronic, progressive condition that involves demyelination of the myelinated neurones in the CNS (oligodendrocytes), caused by an inflammatory process involving activation of immune cells against the myelin.
The inflammatory plaques are disseminated in space and time (occur at multiple sites with >30days between attacks)

Typically presents in young adults (20-40) and more common in women

Relapsing-remitting: most common. Acute attacks followed by periods of remission.

Secondary progressive: relapsing-remitting patients who have deteriorated and have developed neurological signs and symptoms between relapses, usually within 15 years of diagnosis. gait and bladder disorders are usually seen.

Primary progressive: progressive deterioration from onset. More common in older people.

107
Q

MS diagnosis

A

Diagnosed by a neurologist.
McDonald Criteria.

Diagnosis can be made on the basis of two or more relapses and either objective clinical evidence of two or more lesions, or objective clinical evidence of one lesion together with historical evidence of a previous relapse

Symptoms have to be progressive over a period of one year to diagnose primary progressive MS

Investigations:
MRI to demonstrate typical lesions, disseminated in time and space
Lumbar puncture can detect oligoclonal bands of IgG in the CSF which arent present in the serum (= CNS inflammation)
Evoked potentials - delayed visual, auditory and somatosensory

Alternative diagnoses should be excluded

108
Q

MS features

A

Visual: optic neuritis (common presenting features), optic atrophy, Uhthoff’s phenomenon (worsening vision following a rise in body temp, eg after bath), internuclear ophthalmoplegia

Sensory: pins and needles, numbness, trigeminal neuralgia, Lhermittes syndrome (paraesthesiae in limbs on neck flexion)

Motor: UMN/spastic weakness (commonly in legs)

Cerebellar: ataxia, tremor

Others: urinary incontinence, sexual dysfunction, intellectual deterioration, fatigue

109
Q

Lhermittes sign

A

Paraesthesia down the spine and into the limbs when flexing the neck.

Indicates disease in the cervical spinal cord in the dorsal column.

Caused by stretching the demyelinated dorsal column

110
Q

Uhthoff’s phenomenon

A

Worsening of symptoms, and worsening of vision when there is a rise in body temperature (eg. after a bath)

111
Q

Management of MS

A

Specialist MDT: neurologists, specialist nurses, physiotherapy, OT

Disease modifying drugs and biologic therapies can induce long term remission

Methylprednisolone during a relapse can shorten a relapse

Symptom control:

  • Spasticity: baclofen or gabapentin
  • Trigeminal neuralgia: carbamazepine
  • Tremor: botulinum toxin
  • Urgency/frequency: intermittent self catheterisation, or tolterodine
  • Fatigue: amantadine, CBT, exercise
112
Q

Types of motor neurone disease

A

Amyotrophic lateral sclerosis (most common): LMN signs in arms and UMN signs in legs

Primary lateral sclerosis: UMN signs only

Progressive muscular atrophy: LMN signs only, affects distal muscles before proximal, carries best prognosis

Progressive bulbar palsy: palsy of the tongue, muscles of chewing/swallowing, and facial muscles due to loss of function of brainstem motor nuclei, carries worst prognosis

113
Q

Motor neuron disease

  • cause
  • features
  • diagnosis
A

Unknown cause
Rare before 40y

Features which point towards MND:

  • Mixture of LMN and UMN signs
  • Fasciculations
  • Absence of sensory signs
  • Wasting of small hand muscles/tibialis anterior

Doesnt affect external ocular muscles, no cerebellar signs, abdominal reflexes are usually preserved and sphincter dysfunction is a late feature

Diagnosis:
Clinical diagnosis
Nerve conduction studies will show normal motor conduction and can help exclude neuropathy
Electromyography shows reduced number of action potentials with increased amplitude
MRI excludes cervical cord compression and myelopathy

114
Q

Management of MND

A

Riluzole: glutamate inhibitor, used mainly in ALS, prolongs life by about 3 months

Respiratory care: NIV (BIPAP) at night, prolongs life by about 7 months

Palliative input

Prognosis: poor. 50% die within 3 years.

115
Q

Cervical spondylosis

  • pathophysiology
  • features
  • management
A

Degeneration of the annulus fibrosus of the cervical spine and osteophyte formation fo the adjacent vertebrae -> narrowing of spinal canal and intervertebral foramina

Features:
Neck stiffness
Crepitus on moving neck
Stabbing or dull arm pain
Forearm/wrist pain
Root compression (radiculopathy)
Cord compression

Mx:
If red flags: Urgent MRI and specialist referral
Analgesia (WHO pain ladder)
Encourage gentle activity
If no improvement in 4-6 weeks, then MRI and consider neurosurgical referral for injections or surgical decompression

116
Q

Cervical radiculopathy

  • what is it
  • features
A

Cervical spinal root compression due to cervical spondylosis
->
Pain/electrical sensations in arms or fingers at the level of the compression, numbness, dull reflexes, LMN weakness, and eventual wasting of muscles innervated by affected root

117
Q

Cord compression as a result of cervical spondylosis

A

UMN signs below the level of the affected root, and LMN signs at the level of the affected root.

weakness, clumsy hands, gait disturbance
UMN leg signs (spastic weakness, upgoing plantars)
LMN arm signs (wasting, hyporeflexia)
Incontinence, hesitancy, urgency

118
Q

Clinical patterns of nerve root impingement:

C5 (C4/5 disc)

A

Weak deltoid and supraspinatus
Reduced supinator jerks
Numb elbow

Pain in neck/shoulder that radiates down front of arm to elbow

119
Q

Clinical patterns of nerve root impingement:

C6 (C5/6 disc)

A

Weak biceps and brachioradialis
Reduced bicep jerk
Numb thumb and index finger

Pain in shoulder radiating down arm below elbow

120
Q

Clinical patterns of nerve root impingement:

C7 (C6/7 disc)

A

Weak triceps and finger extension
Reduced triceps jerk, numb middle finger

Pain in upper arm and dorsal forearm

121
Q

Clinical patterns of nerve root impingement:

C8 (C7/T1 disc)

A

Weak finger flexors and small muscles of the hand
Numb 5th and ring finger

Pain in upper arm and medial forearm

122
Q

Causes of myopathies

A

Inflammatory: polymyositis
Inherited: duchenne/becker muscular dystrophy, myotonic dystrophy
Endocrine: Cushing’s, thyrotoxicosis
Alcohol

123
Q

Duchenne muscular dystrophy

  • cause
  • mutation
  • features
A

X-linked recessive mutation in the gene encoding dystrophin

Frameshift mutation resulting in one or both of the binding sites being lost, leading to a severe form

Progressive proximal muscle weakness from 5 years
Calf pseudohypertrophy
Gower’s sign: child uses arms to stand up from a squatted position
30% have intellectual impairment

124
Q

Becker muscular dystrophy

  • cause
  • mutation
  • features
A

X-linked recessive mutation in the gene encoding dystrophin

Non-frameshift insertion in the dystrophin gene resulting in both binding sites being preserved leading to a milder form

Similar features to duchennes but milder form
Proximal muscle weakness from 10 years
Intellectual impairment less common

125
Q

Investigations for myopathies

A

ESR, CK, AST, LDH - all raised

Electromyography

Tests relevant to systemic causes (eg. TFTs)

Muscle biopsy and genetic testing

126
Q

Pathway of the facial nerve

A

The facial nerve exits the brainstem at the cerebellopontine angle. It passes through the temporal bone and parotid gland where it terminates into its 5 branches:
temporal, zygomatic, buccal, marginal mandibular, cervical

127
Q

functions of the facial nerve

A

Motor: facial expression, stapedius in the inner ear, some muscles in the neck

Sensory: taste from the anterior 2/3 of the tongue

Parasympathetic: submandibular and sublingual salivary glands, and the lacrimal gland

128
Q

UMN vs LMN facial nerve palsy

A

Each side of the forehead has UMN innervation by both sides of the brain
Each side of the forehead has LMN innervation from one side of the brain.

UMN lesions (stroke) -> forehead will be spared and the patient can move their forehead on the affected side.

LMN lesions (bells palsy) -> forehead will not be spare and the patient cannot move their forehead on the affected side

129
Q

Bells palsy

  • cause
  • incidence
  • features
  • mx
  • prognosis
A

Idiopathic
Unilateral LMN facial nerve palsy

Peak incidence 20-40yrs, more common in pregnant women

Features: unilateral facial weakness, forehead affected, post-auricular pain, altered taste, dry eyes, hyperacusis

If patients present within 72 hours of symptoms, consider prednisolone
Patients also require lubricating eye drops and tape eye closed at night

Prognosis: majority recover over several weeks, but may take up to 12 months. Some are left with residual weakness

130
Q

Causes of unilateral facial nerve palsies

A

UMN: stroke

LMN: bell’s palsy, Ramsay-Hunt, acoustic neuroma, parotid tumours, HI, MS, DM

131
Q

Causes of bilateral facial nerve palsy

A

Sarcoidosis, Guillain-Barre syndrome, Lyme disease, bilateral acoustic neuromas (neurofibromatosis type 2)

132
Q

Ramsay-Hunt syndrome

A

Caused by Herpes-Zoster virus
Unilateral facial nerve palsy

Painful and tender vesicular rash in the ear canal, pinna and around the ear on the affected side
Rash can extend to the anterior two thirds of the tongue and hard palate

Treatment should be initiated within 72 hours: prednisolone and aciclovir
+lubricating eye drops

133
Q

Signs caused by space-occupying lesions

A

Raised ICP: headache worse on waking, lying down, bending forward or coughing. vomiting, papilloedema, reduced GCS

Seizures

Evolving focal neurology

Subtle personality change (irritability, lack of initiative, socially inappropriate)

134
Q

Localising focal neurological features to a space-occupying lesion

A

Temporal lobe: dysphasia, contralateral homonymous hemianopia, amnesia

Frontal: hemiparesis, personality change, grasp reflex, brocas dysphasia, unilateral anosmia, perseveration, executive dysfunction, reduced verbal fluency

Parietal: hemisensory loss, reduced two point discrimination, unable to recognise an object by touch alone, sensory inattention, dysphasia

Occipital: contralateral visual field defects, persisting images once the stimulus has left the field of view (palinopsia), polyopsia (seeing multiple images)

Cerebellum (DANISH): dysdiadochokinesia, ataxia, nystagmus, intention tremor, slurred speech, hypotonia

135
Q

Causes of space-occupying lesions in the brain

A 
Primary tumour: astrocytoma, glioblastoma, oligodendroglioma, meningioma, primary CNS lymphoma
Brain mets: breast, lung, melanoma
Aneurysm
Abscess
Chronic subdural haematoma
Granuloma
Cyst
136
Q

Tumour management

A

Benign: surgical excision if possible
Malignant: hard to resect, but excise if possible. Debulking radiotherapy pre-op. Chemo-radiotherapy post-op

Seizure prophylaxis
Treat any headache with analgesia

Treat cerebral oedema with dexamethasone (mannitol if acute rise in ICP)

137
Q

Acoustic neuroma/ vestibular schwannoma

  • what is it
  • features
  • associated condition
  • Ix
A

Tumour of the schwann cells surrounding the auditory nerve of CNVIII
They occur around the cerebellopontine angle and may compress other nerves (CNV, CNVII)

Features: vertigo, hearing loss, tinnitus and an absent corneal reflex, facial nerve palsy

Bilateral acoustic neuromas are seen in neurofibromatosis type 2

-Ix: MRI of the cerebellopontine angle

138
Q

Wernicke’s aphasia

A

Receptive aphasia, due to a lesion of the superior temporal gyrus. typically supplied by the inferior division of the left MCA

Lesions result in sentences that make no sense, word substitution and neologisms but speech remains fluent.

Comprehension is impaired

139
Q

Broca’s aphasia

A

Expressive aphasia. Due to a lesion of the inferior frontal gyrus. Typically supplied by the superior division of the left MCA.

Speech is non-fluent, laboured, and halting.
Comprehension is normal

140
Q

Conduction aphasia

A

Classically due to a stroke affecting the arcuate fasciculus (connects wernickes and brocas)

Speech is fluent but repetition is poor
Aware of errors they are making
Comprehension is normal

141
Q

Different types of ataxia caused by lesions to different areas of the cerebellum

A

Cerebellar hemisphere lesions cause peripheral ataxia (finger-nose ataxia)

Cerebellar vermis lesions cause gait ataxia

142
Q

Contents of the cavernous sinus

A

Contents of the sinus: internal carotid artery, abducens nerve

Lateral wall components: CNIII, CNIV, CNV1, CNV2

143
Q

Causes of cerebellar syndrome

A

Friedreich’s ataxia, ataxia telangiectasia, neoplastic (cerebellar haemangioma), stroke, alcohol, multiple sclerosus, hypothyroidism, drugs (phenytoin, lead poisoning), paraneoplastic (secondary to lung cancer)

144
Q

Cerebral perfusion pressure

A

Mean arterial pressure - intracranial pressure = cerebral perfusion pressure

the net pressure gradient causing blood flow to the brain. Tightly autoregulated.

A sharp rise in CPP can cause raised ICP, and a fall in CPP can cause ischaemia

145
Q

Circulation of CSF

A

Produced by the ependymal cells in the choroid plexus or in the blood vessels. It travels to the lateral ventricles via the foramen of munro, then to the third ventricle, then through the cerebral aqueduct into the 4th ventricle, and then into the subarachnoid space, where it is reabsorbed into the venous system via arachnoid granulations into superior sagittal sinus

146
Q

Vol of CSF in the brain

Vol of CSF produced

A

150ml in the brain

500ml produced by ependymal cells in the choroid plexus or blood vessels

147
Q

Charcot-Marie-Tooth disease

  • what is it
  • features
  • management
A

most common inherited peripheral neuropathy

Predominantly motor loss

features: sprained ankles, foot drop, high arched feet, hammer toes, distal muscle weakness, distal muscle atrophy, hyporeflexia, stork leg deformity

No cure, management is focused on physical and occupational therapy

148
Q

Common peroneal nerve lesion

A

Occurs at the neck of the fibula

Features: foot drop, week dorsiflexion, weak foot eversion, weakness of extensor hallucis longus, sensory loss over dorsum of foot and lower lateral part of leg, wasting of the anterior tibial and peroneal muscles

149
Q

Cranial nerve reflexes afferent and efferent limbs

  • Corneal
  • Jaw jerk
  • Gag
  • Carotid sinus
  • Pupillary light
  • Lacrimation
A
  • Corneal: ophthalmic nerve (V1), facial nerve (VII)
  • Jaw jerk: mandibular (V3), mandibular (V3)
  • Gag: glossopharyngeal (IX), vagal (X)
  • Carotid sinus: glossopharyngeal (IX), vagal (X)
  • Pupillary light: optic (II), oculomotor (III)
  • Lacrimation: ophthalmic (V1), facial (VII)
150
Q

Creutzfeldt-Jakob disease

  • what happens
  • features
  • different types
  • investigations
A
  • Rapidly progressive neurological condition caused by prion proteins, which induce formation of amyloid folds resulting in tightly packed beta-pleated sheets resistant to proteases
  • Features: rapid onset dementia, myoclonus
  • Sporadic: 85% of cases, some are familial, mean age of onset 65
  • New variant: average onset 25, median survival 13 months. Psychological symptoms (anxiety, withdrawal, dysphonia)

-Ix: CSF is usually normal, EEG (biphasic, high amplitude sharp waves in sporadic CJD), MRI (hyperintense signals in the basal ganglia and thalamus)

151
Q

Encephalitis

  • pathophysiology
  • features
  • ix
  • mx
A

-HSV-1 responsible for most adult cases, typically affects temporal and inferior frontal lobes

-Features: fever, headache, psychiatric symptoms, seizures, vomiting, focal features
Peripheral lesions have no relation to presence of HSV encephalitis

  • Ix:
  • CSF: lymphocytosis, elevated protein
  • PCR for HSV
  • CT: medial temporal and inferior frontal changes
  • MRI is better than CT
  • EEG: lateralised periodic discharges at 2 Hz

-Mx: IV aciclovir

152
Q

Friedreich’s ataxia vs ataxia telangiectasia

A

Friedreichs: autosomal recessive, cerebellar ataxia, onset 10-15yrs, kyphoscoliosis, HOCM, DM, optic atrophy

Ataxia telangiectasia: autosomal recessive, cerebellar ataxia, onset 1-5 years, increased risk of lymphoma and leukaemia, IgA deficiency (infections), telangiectasia

153
Q

Guillain-Barre syndrome

  • what is it
  • pathophysiology
A

Immune mediated demyelination of peripheral nervous system, often triggered by infection

Pathophysiology: cross reaction of antibodies with gangliosides in the peripheral nervous system. Correlation between anti-ganglioside antibodies (anti-GM1) and clinical features has been demonstrated

Associated with campylobacter jejuni, cytomegalovirus and Epstein-Barr virus

154
Q

Guillain-barre syndrome features

A 
Progressive weakness of all four limbs
Classically ascending (lower extremities affected first), but proximal affected earlier than distal

Sensory symptoms tend to be mild

Other features: history of gastroenteritis, areflexia, cranial nerve involvement, autonomic involvement (urinary retention, diarrhoea)

Less common features: papilloedema

155
Q

Investigations for guillain-barre syndrome

A

Lumbar puncture: rise in protein with a normal WCC

Nerve conduction studies

156
Q

Management and prognosis of Guillain-Barre

A

Mx: IV immunoglobulins, plasma exchange, supportive care, VTE prophylaxis (PE common), intubation and ventilation due to resp failure

Prognosis: symptoms usually start within 4 weeks of preceding infection. Symptoms peak within 2-4 weeks and then there is a recovery period that can last months-years

157
Q

Huntington’s disease

  • cause/pathophysiology
  • prognosis
A

Inherited neurodegenerative condition
Progressive and incurable
Typically results in death 20 years after onset of symptoms

Autosomal dominant
Degeneration of cholinergic and GABAergic neurons in the striatum of the basal ganglia

158
Q

Features of Huntington’s

A 
Chorea
Personality changes (irritability, apathy, depression)
Intellectual impairment
Dystonia
Saccadic eye movements
Speech difficulties
Swallowing difficulties

Genetic anticipation: successive generations have more repeats in the gene, resulting in earlier age of onset and increased severity of disease

159
Q

Idiopathic intracranial hypertension

  • risk factors
  • features
  • management
A
  • Risk factors: young overweight females, pregnancy, drugs (OCP, steroids, tetracycline, vit A, lithium)
  • Features: headache, blurred vision, papilloedema, enlarged blind spot, CNVI palsy
  • Mx: weight loss, diuretics (acetazolamide), topiramate, repeated LP, optic nerve sheath decompression and fenestration, lumboperitoneal or ventriculoperitoneal shunt
160
Q

Meralgia paraesthetica

A

Mononeuropathy
Lateral cutaneous nerve of the thigh (L2-L3)
Anterolateral burning thigh pain from entrapment under the inguinal ligament

161
Q

Internuclear ophthalmoplegia

A

Impaired adduction of the ipsilateral eye with horizontal nystagmus of the abducting eye on the contralateral side

Due to a lesion in the medial longitudinal fasciculus, which connects the cranial nuclei of CNIII, CNIV, and CNVI

Seen in MS and vascular disease

162
Q

Cavernous sinus thrombosis

A

Periorbital oedema
Ophthalmoplegia
Trigeminal nerve involvement
Central retinal vein thrombosis

163
Q

Lambert-Eaton syndrome

  • associated condition
  • cause
  • features
  • EMG features
  • Mx
A

Associated with small cell lung cancer

Antibodies directed against presynaptic voltage-gated calcium channels in the peripheral nervous system

Features: repeated muscle contractions lead to increased muscle strength (opposite of MG), limb-girdle weakness, hyporeflexia, autonomic symptoms

EMG: incremental response to repetitive electrical stimulation

Mx: treat underlying cancer, immunosuppression with prednisolone or azathioprine, IV Ig and plasma exchange may be beneficial

164
Q

Meningitis

  • common causes in adults
  • symptoms
  • signs
  • neurological sequelae
A
  • Meningococcus, pneumococcus
  • Symptoms: headache, fever, N+V, photophobia, drowsiness, seizures
  • Signs: neck stiffness, purpuric rash
  • Neurological sequelae: sensorineural hearing loss, epilepsy, paralysis, intracerebral abscess, sepsis, brain herniation, hydrocephalus
165
Q

CSF findings in meningitis

  • bacterial: appearance, glucose, protein, WCC
  • viral: appearance, glucose, protein, WCC
  • TB: appearance, glucose, protein, WCC
A
  • bacterial: appearance cloudy, glucose low (1/2 of plasma), protein high, WCC high
  • viral: appearance clear/cloudy, glucose 60-80% of plasma, protein normal/raised, WCC high but less high than bacterial
  • TB: appearance slightly cloudy/ fibrin web, glucose low (1/2 of plasma), protein high, WCC not as high as bacterial
166
Q

Management of meningitis

A

Pre-hospital antibiotics before transfer: IM benzylpenicillin

Empirical therapy <3m: IV cefotaxime and amoxicillin
Empirical therapy 3m-50y: IV cefotaxime
Empirical therapy >50: IV cefotaxime and amoxicillin

Meningococcal meningitis: IV benzylpenicillin of cefotaxime
Pneumococcal meningitis: IV cefotaxime
H influenze meningitis: IV cefotaxime
Listeria meningitis: IV amoxicillin + gentamicin

Dexamethasone IV should be given to reduce risk of neuro sequelae
Prophylaxis should be given to contacts

167
Q

Investigations for meningitis

A 
FBC
CRP
Coagulation screen
Blood culture
Whole-blood PCR
Blood glucose
Blood gas

Lumbar puncture if no signs of raised ICP

168
Q

Myaesthenia gravis

  • what is it
  • associated conditions
A

Autoimmune antibodies against acetylcholine receptors

Associated conditions: thymomas, thymic hyperplasia, autoimmune (pernicious anaemia, autoimmune thyroid disorder, RA, SLE)

169
Q

Features of myaesthenia gravis

A

Fatiguability (muscles become progressively weaker during periods of activity)
Extraocular muscle weakness (diplopia)
Proximal muscle weakness (face, neck, limb girdle)
Ptosis
Dysphagia

170
Q

Investigations for myaesthenia gravis

A

Single fibre electromyography (high sensitivity)
CT thorax to exclude thymoma
Creatine kinase is normal
Autoantibodies (antibodies to ACh receptors, or anti-muscle-specific tyrosine kinase antibodies)
Tensilon test: IV endrophonium reduces muscle weakness temporarily

171
Q

Management of myaesthenia gravis

A

Long acting acetylcholinesterase inhibitors (pyridostigmine)
Immunosuppression (prednisolone)
Thymectomy

172
Q

Myaesthenic crisis

  • what is it
  • management
A

Life-threatening weakness of respiratory muscles during a relapse.
Mx: Plasmapharesis, IV immunoglobulins, may require ventilatory support

173
Q

Side effects of myaesthenia gravis treatment

A

Pyridostigmine is an acetylcholinesterase inhibitor.
Gives cholinergic side effects: incresaed salivation, lacrimation, swaets, vomiting, miosis

May have a cholinergic crisis

174
Q

Exacerbating factors of myaesthenia gravis

A 
Exertion
Pregnancy
Hypokalaemia
Infection
Change of climate
Emotion
Drugs: penicillamine, quinidine, procainamide, beta blockers, lithium, phenytoin, antibiotics (gentamicin, macrolides, quinolones, tetracyclines)
175
Q

Neurofibromatoses

  • inheritance
  • type 1 features
  • type 2 features
A

Both autosomal dominant

Type 1: cafe-au-lait spots (>6, 15mm diam), axillary/ groin freckles, peripheral neurofibromas, iris haematoma, scoliosis, phaeochromocytoma

Type 2: bilateral acoustic neuromas, multiple intracranial schwannomas, meningiomas, and ependymoma

176
Q

Normal pressure hydrocephalus

  • what is it and what is it caused by
  • triad of symptoms
  • investigations
  • management
A

Reversible cause of dementia
Secondary to reduced CSG absorption at the arachnoid villi
May be secondary to head injury, SAH or meningitis

Triad: urinary incontinence, dementia, gait abnormality (wet, wacky and wobbly)

Investigations: CT head or MRI head will show hydrocephalus with an enlarged fourth ventricle

management: ventriculoperitoneal shunting

177
Q

Peripheral neuropathies which predominantly cause motor loss

A

Guillain-Barre syndrome
Porphyria
Lead poisoning
Hereditary sensorimotor neuropathies (Charcot-Marie-Tooth)
Chronic inflammatory demyelinating polyneuropathy
Diphtheria

178
Q

Peripheral neuropathies which predominantly cause sensory loss

A

Diabetes, uraemia, leprosy, alcoholism, vit B12 deficiency, amyloidosis

179
Q

Features of post-lumbar puncture headache

A

Typically occurs in young females with a low BMI
Usually develops 24-48 hours following an LP but may occur a week later
May last several days
Worsens with upright position
Improves with recumbent position

180
Q

Management of post-lumbar puncture headache

A

Supportive (analgesia, rest)
If pain continues for >72 hours then a specific treatment is indicated in order to prevent subdural haematoma
Treatment option: blood patch, epidural saline, IV caffeine

181
Q

Which roots are tested during the following reflexes -

  • ankle
  • knee
  • biceps
  • triceps
A
  • ankle: S1-S2
  • knee: L3-L4
  • biceps: C5-C6
  • triceps: C7-C8
182
Q

Brown-Sequard syndrome

  • Cause
  • Tracts affected
  • Clinical features
A
  • Spinal cord hemisection
  • Tracts affected: lateral corticospinal tract, dorsal columns, lateral spinothalamic tract

-Features:
=Ipsilateral spastic paralysis below the lesion (UMN lesion affecting corticospinal tract)
=Ipsilateral loss of proprioception and vibration sensation (DCML tract)
=Contralateral loss of pain and temperature sensation (lateral spinothalamic tract)

183
Q

Subacute combined degeneration of the spinal cord

  • cause
  • tracts affected
  • clinical features
  • complication if not treated
  • Which other condition has these same features (in addition to cerebellar ataxia/DANISH)
A
  • Vitamin B12 deficiency
  • Tracts affected: the dorsal and lateral columns -> lateral corticospinal tracts, spinocerebellar tracts, dorsal column medial lemniscus

-Features:
=Bilateral spastic paralysis (corticospinal tracts)
=Bilateral loss of proprioception and vibration sensation (DCML)
=Bilateral limb ataxia (spinocerebellar)

Joint position and vibration sense is lost first and then distal paraesthesia
UMN signs in the legs: extensor plantars, brisk knee reflexes, absent ankle jerks

If untreated, stiffness and weakness persists

-Friedreich’s ataxia also presents in this way, with the addition of cerebellar ataxia (DANISH)

184
Q

Anterior spinal artery occlusion

  • spinal tracts affected
  • clinical features
A

-Tracts affected: lateral corticospinal tracts, lateral spinothalamic tracts

-Features:
=Bilateral spastic paralysis (corticospinal)
=Bilateral loss of pain and temperature sensation (spinothalamic)

185
Q

Syringomyelia

  • what is it
  • what is syringobulbia
  • causes
  • typical presentation
  • what causes the presentation
  • other features
  • investigations
  • management
A

Collection of CSF within the spinal cord
Syringobulbia is a fluid-filled cavity within the medulla of the brainstem. Often an extension of the syringomyelia.

Causes: chiari malformation (strong association), trauma, tumours, idiopathic

Presentation: cape-like (neck and arms) distribution of loss of sensation to pain and temperature (lateral spinothalamic), but preservation of light touch, proprioception and vibration (DCML)

Due to the crossing of the spinothalamic tracts in the anterior commissure of the spinal cord being the first tracts to be affected

Other features: spastic weakness (mostly upper limbs), paraesthesia, neuropathic pain, upgoing plantars, bowel and bladder dysfunction
Scoliosis will occur over a matter of years if untreated

Ix: full spine MRI with contrast to exclude tumour or tethered cord
Brain MRI to exclude chiari malformation

Mx: treat the cause of the syrinx. If syrinx is persistent or symptomatic, a shunt can be placed into the syrinx

186
Q

Trigeminal neuralgia

  • what is it
  • features
  • causes/ associated conditions
  • management
A

Unilateral electric shock-like pains, abrupt in onset and termination, limited to one of more divisions of the trigeminal nerve

Often evoked by light touch, including brushing teeth and talking
Frequently occurs spontaneously

Idiopthic, compression of trigeminal roots by tumours/ vascular problems, multiple sclerosus

Management: carbamazepine is first line

187
Q

Trigeminal neuralgia red flags suggesting a serious underlying cause

A

Sensory changes
Deafness and other ear problems
History of skin or oral lesions that could spread perineurally
Pain only in the ophthalmic division of the trigeminal nerve, or bilaterally
Optic neuritis
Family history of multiple sclerosis
Age of onset before 40 years

188
Q

Tuberous sclerosus

  • inheritance
  • cutaneous features
  • neurological features
  • other features
A
  • Autosomal dominant
  • Cutaneous features: ash-leaf spots, roughened patches of skin over lumbar spine, angiofibromas over the nose, fibromata beneath the nail, cafe-au-lait spots
  • Neuro: developmental delay, epilepsy, intellectual impairment
  • Others: retinal hamartomas, gliomatous changes in the brain lesions, polycystic kidneys, lung cysts, heart lesions
189
Q

Wernicke’s encephalopathy

  • causes
  • triad of features
  • other features
  • investigations
  • management
  • complication
A
  • Causes: thiamine deficiency (alcoholics most commonly, or persistent vomiting, stomach cancer, dietary deficiency)
  • Triad: ophthalmoplegia/ nystagmus, ataxia, confusion
  • Other features: peripheral sensory neuropathy, altered GCS, petechial haemorrhages in the brain
  • Ix: MRI, decreased red cell transketolase
  • Mx: urgent replacement of thiamine
  • Complication: Korsakoff syndrome
190
Q

Korsakoff syndrome

A

Occurs if Wernicke’s encephalopathy is not treated with thiamine urgently

Korsakoff syndrome = Wernicke’s triad (ophthalmoplegia/ nystagmus, ataxia, confusion) + antero-retrograde amnesia and confabulation

191
Q

What is coning?

A

Herniation of the cerebral tonsils through the foramen magnum, resulting in compression of the brainstem. Occurs when there is a rise in ICP and shifts in CSF

Grave sign and usually indicates a neurosurgical emergency requiring intervention

Can cause Cushings reflex if not treated (hypertension, bradycardia, altered respiration)

192
Q

Types of brain herniations

  • subfalcine
  • central
  • transtentorial/ uncal
  • tonsillar
  • transcalvarial
A
  • Subfalcine: displacement of cingulate gyrus under the falx cerebri
  • Central: downward displacement of the brain
  • Transtentorial/ uncal: displacement of the uncus of the temporal lobe under the tentorium cerebelli -> ipsilateral fixed dilated pupil due to parasympathetic compression of CNIII, and contralateral paralysis due to compression of the cerebral peduncle
  • Tonsillar: displacement of the cerebellar tonsils through the foramen magnum (coning). In raised ICP this causes compression of the brainstem (cardioresp centre), will lead to cushings reflex
  • Transcalvarial: occurs when brain is displaced through a defect in the skull
193
Q

Why do you get Cushing’s reflex symptoms?

A

HTN: the brain autoregulates its own blood supply. As ICP rises, the systemic circulation will change in order to meet the perfusion needs of the brain, resulting in HTN.

Bradycardia and altered respiration: As ICP rises further, the brainstem will be compressed which is where the cardiorespiratory centre is located.

194
Q

Two types of hydrocephalus and their causes

A

Obstructive (non-communicating) and non-obstructive (communicating)

Obstructive: due to a structural pathology blocking the flow of CSF -> leads to dilation of the ventricular system proximal to the site of obstruction
Causes: tumour, acute haemorrhage, developmental abnormalities

Non-obstructive: due to an imbalance of CSF production and absorption. Either caused by increased production (choroid plexus tumour) or reduced absorption (meningitis, post-haemorrhagic)

195
Q

Hydrocephalus investigations

A

CT head is first line
MRI may be used to investigate in more detail
Lumbar puncture is diagnostic and therapeutic

Lumbar puncture must not be used in obstructive hydrocephalus since the difference of cranial and spinal pressure induced by the drainage of CSF will cause brain herniation

196
Q

Management of hydrocephalus

A

External ventricular drain is used in acute, severe hydrocephalus (typically inserted into the right lateral ventricle and drains into a bag at the bedside)

Ventriculoperitoneal shunt is a long term CSF diversion that drains CSF from the ventricles to the peritoneum

If obstructive, the treatment may involve surgical removal of the obstruction

197
Q

Clinical features of hydrocephalus

  • in adults
  • in infants
A 
Symptoms due to raised ICP
Headache (worse in the morning, when lying down and during valsalva)
N+V
Papilloedema
Coma

Infants may have an increased head circumference as their sutures have not fused, they will also have a bulging anterior fontanelle. Children with severe hydrocephalus may have sunsetting eyes (failure of upward gaze) due to compression of the superior colliculus of the midbrain

198
Q

Causes of cerebellar dysfunction

A 
Tumours
MS
Vascular – haemorrhagic or ischaemic
Infections – abscess, prion disease, viral encephalitis
Toxins – anticonvulsants, alcohol
Metabolic- myxoedema, vitamin deficiency 
Trauma
Multiple system atrophy
Developmental deformities
Inherited cerebellar ataxia
199
Q

Gait disorders

  • Hemiplegic
  • Diplegic
  • Festinant
  • Ataxic
  • Neuropathic
  • Antalgic
  • Trendelenburg
A
  • Hemiplegic: spastic lower limb is held out in extension, so move by abduction and circumduction
  • Diplegic: same as hemiplegic but bilateral. Scissoring gait
  • Festinant: parkinsonian. Stooped forward, shuffling, slow to initiate and then gets quicker, slow to turn around, reduced arm swing on one side
  • Ataxic: broad-based, staggers, looks drunk
  • Neuropathic: common peroneal nerve damage causes footdrop and a high steppage gait to clear the toes off the ground
  • Antalgic: painful, reduced stance phase on affected limb
  • Trendelenburg gait: weakness in proximal muscles of lower limb girdle, weak gluteal muscles cannot stabilise the weight-bearing hip, causing the opposite hip and trunk to droop towards the leg in swing phase
200
Q

Cauda equina

  • causes
  • presentation
  • investigations
  • management
  • complications
A
  • Causes: herniation of lumbar disc most common at L4/L5 and L5/S1, tumours, truama, infection, congenital (spina bifida)
  • Presentation: lower back pain, urinary incontinence/retention, reduced sensation in perianal area, decreased anal tone, lower limb motor weakness and sensory deficit
  • Ix: clinical diagnosis. MRI spine
  • Mx: immobilise spine, surgical removal or blood/fragments/tumour/etc, lesion debulking for space occupying lesion, radiotherapy if surgery not appropriate
  • Complications: paralysis, sensory abnormalities, bladder/bowel/sexual dysfunction
201
Q

Decussation of the corticospinal tracts

A

Descending motor tract
Decussates at the lower medulla

Lesion above the medulla = contralateral weakness
Lesion below the medulla = ipsilateral weakness

202
Q

Decussation of the DCML

A

Ascending sensory tract for proprioception, two point discrimination, light touch, vibration

Decussates at the gracile and cuneate nuclei in the medulla
Sacral fibres are more medial and cervical fibres are more lateral

203
Q

Decussation of spinothalamic tract

A

Ascending sensory tract for pain and temperature

Decussates one or two spinal levels higher

Sacral fibres are more lateral and cervical fibres are more medial

Medicine (15 decks)

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