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Y4 Neuro and SS > Neurology > Flashcards

Neurology Flashcards

1
Q

Describe the clinical features of raised ICP? (9)

A
  • Headache
  • Altered mental state (lethargy, irritability, slow decision making, abnormal behaviour)
  • Papilloedma
  • Vomiting (progresses to projectile)
  • Pupil changes: irregular or dilated in one eye)
  • Cranial nerve palsies (esp unilateral ptosis, III or IV lesions)
  • Later changes: hemiparesis, raised BP, bradycardia
  • Seizures, syncope if acute rise in ICP
  • Cushings reflex
  • visual changes: black spots, blurring, enlarged blind spot and reduced peripheral vision (subacute) or reduced central vision and visual acuity (acute advanced)
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2
Q

Describe the headache of raised ICP

A

nocturnal, starting on waking, worse on coughing/ moving

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3
Q

Describe what papillodema looks like

A

blurring of disc margins, loss of venous pulsations, flame haemorrhages

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4
Q

What is the cushings reflex and why does it occur?

A

hypertension + bradycardia + low resp rate due to: Ischaemia at medulla causing sympathetic activation so rise in BP + tachycardia// Baroreceptors detect increase in BP causing Bradycardia// Ischemia @ pons/ medulla resp centers so low resp rate

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5
Q

How should raised ICP be investigated?

A
  • CT/ MRI for underlying lesions
  • blood glucose, renal function and osmolality
  • check for signs of CSF leak
  • ICP monitoring can be done
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6
Q

Give 6 causes of raised ICP

A
  • localised mass lesions (eg traumatic haematoma)
  • neoplasms (glioma, meningioma, mets)
  • abscesses
  • focal odema secondary to trauma, infection or infarction
  • disturbance of CSF circulation
  • major venous sinus thombosis/ obstruction
  • diffuse brain odema/ swelling
  • idiopathic intracranial hypertension
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7
Q

Give 5 causes of diffuse brain odema/ swelling

A
  • meningitis
  • encephalitis
  • diffuse brain injury
  • sub arachnoid haemorrhage
  • reyes syndrome
  • water intoxication
  • cerebral venous thrombosis
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8
Q

Describe the first line steps to management of raised ICP?

A
  • stabilise ABC
  • treat seizures with lorazepam +/- phenytoin
  • Head CT if meets criteria
  • assess C spine, immobilise and order neck CT if not cleared
  • involve neurosurgery
  • head elevation to 30 degrees
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9
Q

When should you intubate someone with a head injury/ raised ICP?

A 
If:
- sats <92%
or
- hypoxic on ABG 
or 
- GCS <8
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10
Q

Describe the further management of someone with raised ICP

A
  • Analgesia with morphine and sedation w/ propofol if necessary
  • mannitol (risk of hypovolaemia) or hypertonic saline if cerebral odema
  • barbiturate coma
  • hypothermia
  • decompressive craniotomy and shunts
  • treat cause (anticoag if venous outflow obstuction, diuretics then shunts if increased CSF, resections/ craniotomys/ steroids for SOLs)
  • hyperventilation (causes hypercapnic vasoconstriction so decreases ICP)
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11
Q

Describe the clinical features of a subarachnoid haemorrhage?

A
  • Sudden onset explosive headache (often occipital) lasting a few seconds or a fraction of a second then a diffuse headache which can last a week or so
  • almost always have N+V
  • altered mental status
  • seizures
  • neck stiffness/ meningism signs sometimes present around 6 hrs after
  • intraocular haemorrhages seen on fundoscopy in 15%
  • other signs of raised ICP
  • 10-15% die before getting to hospital
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12
Q

What warning symptoms may occur prior to SAH as aneurysm expands and bleeds slightly (sentinel bleeds)?

A
  • headache
  • dizziness
  • orbital pain
  • diplopia
  • ptosis
  • sensory or motor disturbance
  • seizures
  • dysphagia
  • bruits less common
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13
Q

Describe the investigation findings consistent with a subarachnoid haemorrhage? (4)

A
  • CT scan without contrast: hyperdense blood vessel in basal cisterns (98% sensitive after 2 hrs and 100% after 6, sensitivity drops after 24hrs)
  • cerebral panangiography then CT or MR angiography if aneurysm found
  • LP if CT scan negative but suspect SAH- spectrophotometry should be able to detect xanthochromia if SAH occured (detected from 12hrs- 2weeks after bleed)
  • ECG changes inc prolonged QT, Q waves, ST elevation
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14
Q

Describe the urgent and supportive management of a SAH? (4)

A
  • stabilise pt and send straight to neurosurgical unit +/- intubation, ventilation, NG tube, analgesia and antiemetics
  • endovascular obliteration by platinum spirals (coiling) or direct neurosurgical clipping to prevent rebleeding
  • oral nimodipine given to prevent vasospasm which leads to cerebral ischaemia/ stroke
  • hydrocephalus can occur as early or late complication, many will resolve on their own but some surgeons drain immediately
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15
Q

Describe the further management of an SAH? (3)

A
  • secondary prevention (stop smoking etc)
  • specialist rehab if lasting impairment
  • antifibrinolytics reduce rate of rebleeding but doesnt improve overall outcomes
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16
Q

Describe the clinical features of meningitis

A
  • Headache
  • Fever
  • Photophobia
  • Neckstifness
  • Vomiting
  • Muscle pains
  • Non blanching purpuric rash
  • seizures
  • altered consciousness
  • Fatigue, muscle pain
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17
Q

What signs require urgent senior review +/- critical care input when managing a meningitis pt? (9)

A
  • rapidly progressive rash
  • poor peripheral perfusion (cap refill >4/ BP >90mmhg)
  • RR <8 or >30
  • HR <40 or >140
  • acidosis <7.3
  • WBC <4
  • lactate >4
  • GCS <12 or drop of 2
  • poor response to initial fluid resus
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18
Q

How should suspected meningitis (meningitis without signs of shock, severe sepsis or signs suggesting brain shift) be managed? (7)

A
  • blood cultures
  • bloods (FBC, renal function, glucose, lactate, clotting, viral PCR, blood gas)
  • LP
  • dexamethasone 10mg IV
  • ceftriaxone IV 2g
  • careful fluid resus
  • throat swab for meningococal culture
  • isolate until abx for 24 hrs, tell microbiology and PH
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19
Q

How should suspected meningitis with signs suggestive of brain shift/ raised ICP, severe sepsis or a rapidly evolving rash be managed? (9)

A
  • critical care input
  • secure airway, give O2
  • take bloods, do cultures
  • fluid resus (if shock/ sepsis/ rapidly evolving rash)
  • ceftriaxone 2g IV
  • Dexamethasone 10mg IV (omit if severe sepsis or rapdily evolving rash)
  • Neuro imagine such as CT head if signs of raised ICP
  • throat swab for meningococcal culture
  • DELAY LP
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20
Q

What tests should be done on CSF when meningitis suspected? (7)

A
  • glucose (w/ concurrent blood glucose)
  • protein
  • microscopy and culture
  • lactate
  • meningococcal and pneumococcal PCR
  • enteroviral, HSV, VZV PCR
  • consider investigations for TB meningitis
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21
Q

What are the criteria for delaying LP in meningitis?

A
  • signs of severe sepsis
  • rapidly evolving rash
  • severe cario/ resp compromise
  • significant bleeding rik
  • signs suggestive of brain compartment shift (do CT first): focal neurosigns, presence of papillodema, continious or uncontrolled seizures, GCS <12
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22
Q

State 5 complications of meningitis

A

septic shock, DIC, septic arthiritis, haemolytic anamia, pericadial effusion, subdural effusion, SIADH, seizures, hearing loss, cranial nerve dysfunction

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23
Q

Describe the clinical features of encephalitis (5)

A
  • bizarre behaviour or confusion
  • decreased GCS or coma
  • fever
  • headache
  • seizures
  • focal neuro signs (weakness, visual disturbance, aphasia, cerebellar signs)
  • history of travel or bite
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24
Q

Describe the key differenced between meningitis and encephalitis?

A
  • Seizures uncommon in meningitis but common in encephalitis
  • photophobia, rash and neck stiffness much more common in meningitis
  • focal neurological signs are a hallmark feature of encephalitis, but only occur in some and later in meningitis
  • mental status is almost always altered in encephalitis, however is common but less so in meningitis
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25
Q

How should encephalitis be investigated?

A
  • bloods: cultures, viral PCR, malaria film biochemistry
  • contrast enhanced CT
  • LP (viral picture usually, if bacterial ?meningitis)
  • EEG: diffuse abnormalities may help confirm encephalitis
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26
Q

Give 3 common viral and 3 common non viral causes of encephalitis

A

Viral: HSV, arbovirus, EBV, CMv, VZV, HIB, mumps (paramyxo), measles, rabies, west nile
Non viral: any bacterial meningitis, lyme disease, TB, malaria, legionella, leptospirosis

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27
Q

How is encephalitis managed?

A
  • start acyclovir within 30 mins or arrival- 10mg/ kg/ 8hrs IV for 14 days as empirical treatment
  • specific therapies exist for CMV and toxoplasmosis
  • supportive therapy in HDU/ ITU if necessary
  • symptomatic treatment with phenytoin if necessary
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28
Q

Define status epilepticus

A

seizure lasting >30 mins or repeated seizures without intervening consciousness - usually in known epilepsy, if 1st presentation then high chance of structural brain lesion

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29
Q

How should status epilepticus be investigated/ assesed?

A
  • bedside glucose (dont miss this as cause) early
  • pulse oximetry and cardiac monitor while its happening
    After treatment started:
  • consider anticonvulsant levels, toxicology, LP, blood cultures, urine cultures, EEG, CT and carbon monoxide levels
  • CXR to evaluate for possible asipration
  • lab glucose, ABG, u&e, ca, fbc, ecg
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30
Q

Describe management of status epilepticus (from start of seizure) (inc paeds and adult doses)

A

0 mins: ABC, high flow O2, check BM, make surroundings safe- (50ml 50% dextrose if hypo)
5 mins: give IV lorazepam 0.1mg/ kg (4mg) slow bolus or rectal diazepam 10-20mg
10-15 mins: (if no response) give 2nd bolus
20-25 mins: phenytoin infusion 20mg/kg (up to 2g) at 50mg/min w/ ECG monitoring AND seek ITU help for general anaesthetic with propofol/ thiopentone if still going at 45 mins

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31
Q

Give 5 causes of spinal cord/ cauda equina compression?

A
  • neoplasms (breast, kindey, thyroid, lung, prostate mets, myeloma or primary bone tumours)
  • trauma
  • infections; abscesses
  • spinal stenosis
  • transverse myelitis
  • disc prolapses (rare but lumbar disc herniations typically cause CES)
  • post op haematoma
  • spondylolithesis
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32
Q

Describe the locations and functions of the 2 main ascending sensory tracts and the main motor tract within the spinal cord

A

Corticospinal tract- lateral cord, ipsilateral motor control
Dorsal column- posterior cord, ipsilateral vibration and proprioception
Spinothalamic tract- anterior cord, contralateral pain, temp and crude touch sensation

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33
Q

What are the upper motor neurone signs?

A
  • Weakness- esp of extensors in arms and flexors in legs
  • Hyperreflexia, clonus, upgoing planters
  • Hypertonia which is spastic (velocity dependent)- clasp knife
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34
Q

What are the lower motor neurone signs

A
  • weakness (pattern consistent with neuronal distribution)
  • muscle wasting
  • fasiculation
  • hypotonia/ flaccidity
  • reflexed reduced or absent
  • flexor planter reflex
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35
Q

Describe the type and distribution of motor and sensory deficit seen with cord lesions

A
  • usually bilateral motor deficit from below level of lesion down- initially LMN signs then UMN over the next hrs.
  • LMN signs + loss of reflexes at the level of the lesion
  • Presence of a sensory level
  • autonomic features may also be present & associated w/ worse prognosis (constipation, retention, incontinence)
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36
Q

Describe the MRC grading of muscle weakness

A 
0= no contraction
1= flicker of contraction 
2= some active movement
3= active movement against gravity
4= active movement against resistance
5= normal power (allowing for age)
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37
Q

Describe the classifications of head injuries?

A
  • Focal (slit into haematoma (sub, extra or intracerebral) or contusion (coup vs contracoup)
    vs
  • Diffuse (concussion vs diffuse axonal injury)
    AND
  • traumatic (split into open/ penetrating vs closed)
    vs
  • non traumatic (axonia, infection, CVA/ TIA, tumour etc)
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38
Q

Describe the pathophy of a concussion

A
  • Stretching of axons causes impaired neurotransmission, ion regulation and reduced blood flow causing temporary brain dysfunction
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39
Q

Describe the clinical features of post concusion syndrome

A

Difficulty thinking clearly, slowed down, confusion, headache, N+V, balance problems, tired, light sensitive, irritable, sad, sleep disturbance, trouble falling asleep

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40
Q

Describe the pathophys of diffuse axonal injury

A
  • Shearing of grey and white matter interface following traumatic acceleration/ deceleration or rotational forces
  • Leads to axonal death so cerebral odema so raised ICP and death
  • they get instate LOC with few recovering- v poor prognosis
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41
Q

State 5 signs of a basilar skull fracture

A

racoon eyes, CSF rhinorrhoea, CSF otorrhoea, battle sign, haemotympanum

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42
Q

Describe the differences in mechanism between extradural (EDH) and subdural (SDH) haemorrhage?

A

EDH: almost always traumatic
SDH: usually traumatic but less major trauma, can be spontaneous also

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43
Q

Describe the difference in presentation between EDH and SDH

A

EDH: young pt, LOC followed by lucid interval then rapid decline in consciousness, signs of raised ICP etc
SDH: acute bleeds can be any age, chronic bleeds seen in elderly, reduced GCS, neuro signs, or chronic bleeds= insidious neurological decline

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44
Q

Where is the bleed for EDH and SDH? What is the radiological appearance?

A

EDH: middle meningeal artery, lentiform shape, limited by suture lines
SDH: bridging veins, cresent shaped, not bound by suture lines but unable to cross midline due to falx cerebri, chronic bleeds appear hypodense- can have acute on chronic

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45
Q

What is the definitive management for EDH and SDH?

A

EDH: urgent craniotomy to relieve raised ICP, if small can just observe
SDH: acute- surgery to relieve raised ICP, if chronic and not causing symptoms then many are left alone

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46
Q

What are the criteria for a head CT within 1 hr of head injury?

A
  • GCS <13 or <15 after 2 hrs
  • focal neuro deficit
  • suspected skull or C spine fracture
  • seizure or vomiting >1 time
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47
Q

What are the criteria for head CT within 8 hrs of head injury?

A 
- LOC or amnesia 
AND 
- age >65 (or)
- coagulopathy (or)
- high impact injury (or)
- retrograde amnesia of > 30 mins
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48
Q

When is a CT neck NOT required to clear the neck and allow mobilisation?

A
  • no posterior midline cervical tenderness
  • no evidence of intoxication
  • pt altert and orientated to person, place, time and event
  • no focal neuro deficit
  • no painful distracting injuries
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49
Q

How do acute bulbar and pseudobulbar palsies present differently?

A
  • A bulbar palsy is one of the nuclei of CN IX- XII (medulla)
  • A true bulbar palsy= LMN lesion (, flacid fassiculating tongue, normal or decreased jaw jerk and reduced gag reflex, quiet nasal speech)
  • corticobulbar palsy/ pseudobulbar palsy is UMN (hot potato speech, increased jaw and palatine reflexes, mood incontinent giggling/ weeping, spastic tongue)
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50
Q

List causes of bulbar and a pseudobular palsies?

A

Bulbar: MND, guillian barre, polio, MG, syringobulbia, brainstem tumours or central pontine demyelinolysis
Pseudobulbar: MS, MND, BILATERAL stroke or centralpontine demyelinolysis

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51
Q

What is epilepsy

A

a tendency to experience seizures- spontaneous, intermittent abnormal electrical activity within the brain

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52
Q

What are the major causes of epilepsy?

A
  • 2/3 are idiopathic
  • structural: scarring from previous brain injury, developmental, SOL, stroke, vascular malformation
  • neurocutaneous syndromes eg. tuberous sclerosis
  • sarcoidosis
  • SLE
  • channelopathies
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53
Q

What reversible factors could provoke seizures and need to be ruled out before diagnosing epilepsy

A
  • alcohol and alcohol withdrawal
  • raised ICP
  • fever
  • metabolic disturbance
  • infection
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54
Q

What general advice should be given to epilepsy pts?

A
  • avoid swimming and heights unsupervised, at least till diagnosis is known
  • inform the DVLA and need to be seizure free for 1 yr until you can drive
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55
Q

What is the difference between generalised and focal/partial seizures?

A

generalised- seizure involving both sides of the brain (always lose consciousnes)
Focal/ partial- seizure activity limited to one or more areas but on one side of the brain

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56
Q

What is the difference between and simple and a complex partial/ focal seizure?

A

Simple- consciousness not lost, lasts <1 min, limited to one muscle group
Complex- consciouness lost, lasts 1-2 mins, post ictal period after, commonly affects temporal lobe

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57
Q

What are the different types of generalised seizures?

A
  • Tonic- clonic
  • Atonic (drop attacks)
  • Myoclonic (quick movements/ sudden jerking, happen in clusters several times a day or several days in a row
  • Absence (brief LOC, may maintain posture but face, eyes or mouth may move, commonest age 4-12, cant recall them)
  • Infantile spasm (before 6 months, when wakening or falling asleep, brief movements in neck, trunk or legs)
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58
Q

Describe the phases to generalised tonic clonic seizures

A
  1. contract: body, arms, legs flex
  2. extend
  3. tremor/ shake
  4. contraction and relaxation of muscles, clonic period
  5. post ictal period: sleepy, vision problems, fatigue, ache, headache
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59
Q

Describe the features of a temporal lobe focal seizure

A
  • automatisms (lip smacking, screaming, crying)
  • dysphagia
  • dejavu
  • emotional disturbance
  • hallucinations of smell, taste, sound
  • delusional behaviours
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60
Q

Describe the clinical features of frontal lobe focal seizures

A
  • motor features such as posturing or peddling legs
  • jacksonians march (starts distal part of limb and spreads to ipsilateral side of face)
  • motor arrest
  • dysphagia or speech arrest
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61
Q

Describe clinical features of parietal and occipital lobe focal seizures

A
  • parietal: sensory disturbance (motor if spread to precentral gyrus)
  • occipital: visual phenomena such as spots, lights and flashes
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62
Q

What drugs are best for focal seizures

A

1st- carbemazepine or lamotrigine

2nd= sodium valproate

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63
Q

What drugs are used for generalised tonic seizures

A 
1st= sodium valproate or lamotrigine
2nd= levetiracetam
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64
Q

What drugs are used for absence, myoclonic or tonic or atonic seizures?

A

1st- sodium valproate

2nd- lamotrigine/ levetiracetam

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65
Q

What general points are important when approaching drug management of epilepsy?

A
  • treat w/ one drug then increase dose
  • if not work, change to another
  • then try combinations
  • stop only if seizure free for 2 yrs, after assessing risk and benefits and do it slowly over 2-6 months
  • COCPs reduce lamotrigines effectivness so may need higher dose
  • many AEDs induce POP metabolism
  • Lamotrigine safest in pregnancy
66
Q

Describe the clinical features of a migraine

A
  • usually one sided at front or side but can be bilateral
  • often starts on one side and spreads
  • often throbbing or pulsatile in nature
  • they cannot carry out activities, need to lie down and do nothing, often in a dark room
  • may get sensory or motor changes, dizziness, blurred vision
  • may be preceeded by aura
  • associated symptoms inc N+V, noise and light intolerance, poor concentration, diarrhoea, abdopain, pallor, sweating
67
Q

Describe aura symptoms which typically occur with migraine

A
  • usually lasts <60 mins and end before headache starts
  • Visual (commonest): usually affect one side of vision and get bigger over 5-20 mins, includes temporary vision loss, bright lights, floaters, objects or letters rotate/ shake
  • sensory: numbness and pins and needles, often start in hand and travel up
  • speech problems
  • odd smells/ tastes and food cravings
68
Q

Give 9 common triggers for migraine

A 
Chocolate
Hangovers 
Orgasms
Cheese and caffiene 
Oral contraceptives 
Lie- ins
Alcohol
Travel
Exercise
69
Q

What are the diagnostic criteria for migraine with out aura?

A

> 4 headaches lasting 4-72 hrs + N/V or photophobia with any 2 of: unilateral, pulsating, impairs or worsened by activity

70
Q

How should migraines be managed during attacks?

A
  • warm/ cold pads may help
  • rebreathing into paper bag can help abort attacks
  • oral triptans (or nasal if 12-17yrs) + NSAIDs or paracetamol
  • anti emetics can help even when no N+V
71
Q

Describe the prophylaxis of migraine

A
  • identify and avoid triggers
  • 1st= propanolol or topimerate (teratogenic and interfers w/ pill)
  • 2nd= amitriptyline
  • 3rd= botulinum toxin type a injections
  • NICE recommends acupuncture if drugs not working
  • some pts may have previously been put on valproate, pregablin, ACEi etc, if these are working then continue
72
Q

State the diagnostic criteria for a medication overuse headache (4)

A

Need to have tension like headache for 15 days or more per month after having taken triptans of opioids for >10 days per month for 3 months or paracetamol/ NSAIDs for 15 days/ month. It also needs to resolve within 2 months of stopping that medication.

73
Q

Describe the management of a medication overuse headache

A

Stop the medication. Theyll usually get get rebound worsening of the headache at 2-10 days. This may require an in pt stay. NSAIDs can be given to help if thats not what they’re hooked on.
Assess for complications of long term analgesics use such as kidney, upper GI and liver damage.
Initial headache will often come back so need to treat that also.

74
Q

Describe the clinical features of a cluster hedache

A
  • Mostly affects men, any age and smokers.
  • Rapid onset excruciating pain around one eye w/ watering, blood shot, lid swelling, flushing, rhinorrhoea, miosis, ptosis. Always unilateral. Lasts 15-180mins, once or twice a day for weeks then pain free period which can last a year or two.
  • Often nocturnal.
  • Restless during attacks
75
Q

How should cluster headaches be managed?

A
  • 100% O2 for 15 mins (can get home O2 for this)
  • sumatriptan SC or zolmitriptan nasal spray at onset are effective
  • verapamil, prednisolone and lithium are good for prevention
  • avoid triggers- commonly alcohol and smoking
  • regular sleep helps many
76
Q

Describe the clinical features of benign intracranial HTN

A
  • Raised ICP in absence of mass lesion or hydrocephalus- thought to be from impaired CSF absorption
  • Almost only in obese women
  • throbbing headache, worst first thing in morning and last at night
  • worse on coughing/ straining/ bending over
  • relieved on standing
  • gradual visual field defects- greying out or black spots on bending or stooping, halos or short episodes of catherine wheel flashes, enlarged blind spot and reduced peripheral vision as with any raised ICP
  • N+V common
77
Q

How should benign intracranial HTN be managed?

A
  • First needs thorough investigation to ensure there isnt underlying cause of raised ICP, inc CT and LP and MRI/ venogram for central venous thrombosis
  • weight reduction and diuretics
  • CSF diversion therapy or serial LPs may be needed for visual disturbance
  • prednisolone can be used acutely to relieve headache and papilodema
78
Q

Give 7 red flags for headaches

A
  • change in pattern of headache
  • new onset over age 50
  • onset of seizures
  • headache with systemic illness
  • personality change
  • symptoms suggestive of raised ICP: morning headaches, headache with coughing, sneezing, straining
  • acute onset of worst headache ever (possible intracranial aneurysm)
  • temporal tenderness
  • photophobia/ neck stiffness
79
Q

Explain the pathophys of idiopathic parkinsons disease

A
  • loss of dopaminergic neurones in substantia nigra
  • leads to increased activity of basal ganglia and so hyperkinesia
  • most are sporadic with many gene loci identified
  • mean onset is in 60s
80
Q

What are the 4 cardinal features of parkinsons?

A
  • TREMOR: worse at rest, pinrolling
  • HYPERTONIA: rigidity (lead pipe- not velocity dependent), when combined with tremour gives cogwheeling during rapid pronation/ supination
  • BRADYKINESIA: slow to initate movement, actions slow and decreased in amplitude with repitition, slow blink rate and micrographia
  • GAIT: shuffling, pitched forward, loss of arm swing, en bloc turning
81
Q

Give 4 other (non cardinal) features of parkinsons

A
  • expressionless face
  • autonomic dysfunction (postural hypotension, constipation, urinary frequency, urgency, drooling)
  • sleep disturbance (REM sleep disorder)
  • reduced sense of smell
  • neurpsychiatric complications: dementia, depression, psychosis
  • signs are almost always worse on one side- if bilateral look for other causes
82
Q

Describe the pharmacological management of parkinsons disease (7)

A
  • Levodopa: efficacy reduced over time so start it late as poss
  • dopa decarboxylase inhibitors (carbidopa/ co benledopa) will increase levo dopa’s efficacy
  • dopamine agonists like ropinerole can help delay starting levodopa in early PD
  • apomorphine: potent DA agonists used to even out end of dose effects or as rescue pen for dose effects
  • anticholinergics: young pts only as confuse old ppl
  • MAO- B inhibitors: alternative to DA’s in early PD
  • COMT inhibitors eg etacapone- help motor complications in late disease and lessen off time in end of dose wearing off
  • clonazepam and melatonin for REM sleep disorder
  • fludrocotisone if postural hypotension
  • quetiapine and clozapine for distressing hallucinations (worsens parkinsons)
  • Acetylcholinesterase inhibitor for dementia (donepezil and rivastigmine)
83
Q

describe the surgcial management options for parkinsons disease

A
  • deep brain stimulation: may help but only if partially dopamine responsive still
  • surgical ablation of basal ganglia circuits eg subthalamic nucleus
84
Q

What are the 4 parkinsons plus syndromes and their other features

A
  • Progressive supranuclear palsy: early postural instability, vertical gaze palsies +/- falls, rigidity of trunk> limbs, symmetrical onset, little tremor, speech and swallowing problems
  • Multiple systems atrophy: early autonomic features eg incontinence, postural hypotension + cerebellar + pyramidal signs, rigidity > tremor
  • Corticobasal degeneration: akinetic rigidity involving one limb, cortical sensory loss, apraxia
  • Lewy body dementia
85
Q

Give 5 secondary causes of parkinsonism

A
  • vascular parkinsonism: diabetic/ HTN pt with postural instability and falls
  • drugs: antipsychotics, metoclopramide
  • toxins: manganese
  • wilsons disease
  • trauma
  • encephalitis
  • neurosyphilis
86
Q

How can you clinically distinguish MND from

other polyneuropathies?

A
  • Both may have mixed UMN and LMN signs
  • There is NO sensory loss or sphincter disturbance in MND
  • It also NEVER effects eye movements- helps distinguish from MG
87
Q

Describe the 2 commonest clinical patterns of MND, state the other two.

A
  • amylotrophic lateral sclerosis (ALS): Loss of motor neurones in motor cortex AND anterior horn of cord (so UMN +LMN signs). Definite if in 3 regions, probably if in 2.
  • Progressive bulbar palsy: bulbar palsy (LMD) , often mixed with pseudobulbar palsy (UMN)
  • progressive muscular atrophy: only affects anterior horn cells so LMN signs only, distal before proximal muscle groups affected
  • primary lateral sclerosis: rare, loss of betz cells in motor cortex, mainly UMN
88
Q

How does MND tend to present and describe its clinical features

A
  • age >40
  • stumbling spastic gain, foot drop +/- proximal myopathy, weak grip, poor shoulder strength or aspiration pneumonia are usually 1st presentations
  • UMN signs AND LMN signs (tongue fasiculation common)
  • frontotemporal dementia occurs in 25%
  • no sensory disturbance, eyes not effected
89
Q

How should suspected MND be investigated?

A
  • no diagnostic test
  • MRI brain/ cord to exclude structural cause
  • LP excludes inflammatory causes
  • neurophysiology studies can detect subclinical denervation and exclude mimicking motor neuropathies
90
Q

Describe the management of MND

A
  • Riluzole: inhibits glutamate release and NMDA receptor antagonist, is the only drug proven to improve survival but only by 2-4 months but has significant impact on tracheostomy free survival
  • Positioning, oral care and anti muscarinic (glycopyrronium) can help with the excess saliva
  • Blended and thickened foods as well as gastrostomy can help with dysphagia
  • Exercise, orthotics can help with spasticity
  • Augmentative and alternative communication equipment can aid comms difficulty
  • Involve palliative care from point of diagnosis as median survival from diagnosis is only 2-4 yrs
  • Positive pressure ventilation can aid with breathing greatly
  • Muscle cramps- quinine, baclofen, gabapentin, diazepam
  • communication aids
  • Early discussion about end of life care are esp important with ALS as many will develop frontotemportal dementia and not be able to express wishes later on in the disease
91
Q

What is Multiple sclerosis?

A
  • inflammatory plaques of demyelination in the CNS (all UMN)
  • disseminated in space and time (ie multiple sites >30 days between attacks)
  • demyelination heals poorly leading to axonal loss and 80% get lasting disability
92
Q

Optic neuritis and intranuclear opthalmoplegia are common in MS and often how it presents initially. Describe these two comditions

A
  • Optic neuritis: pain on eye movement, reduced central vision, red desensitisation- esp centrally, usually unilateral, sometimes swollen disc on fundoscopy acutely and after the disc appears white (scarred), RAPD
  • Intranuclear ophthalmoplegia (MLF syndrome)- when one eye looks laterally the other doesn’t turn medially or lags, often with nystagmus of the laterally moved eye, due to demyelination of medial longitudinal fasciculus connecting the IV and VI cranial nerves in the brain stem, can be bilateral
93
Q

Other than intranuclear opthalmoplegia and optic neuitis, give 7 other deficits commonly caused by MS and state when the symptoms tend to get worse

A
  • worsen with heat (hot weather, shower, bath)
  • SENSORY: dysaesthsia, pins n needles, decreased vibration sense, trigeminal neuralgia
  • MOTOR: spastic weakness, myelitis, CN palsies-> diplopia
  • SEXUAL/ GU: ED, incontinence, urinary retention
  • EYE: diplopia, hemianopia, pupil defects, visual phenomena on exercise
  • cerebellum signs
  • cognitive: visual spacial neglect, accidnet, low mood, poor executive functioning
94
Q

How is MS diagnosed?

A
  • clinical- McDonald criteria can be used
  • MRI sensitive but not specific for detecting lesions and can help exclude other causes
  • oligoclonal bands of IgG on electrophoresis of CSF can help indicate MS
95
Q

How should relapsing remitting and primary and secondary progressive MS be managed?

A
  • Regular exercise, stop smoking and avoid stress may help
  • Legal obligation to inform DVLA
  • Dimethyl fumarate then interferon B for mild- moderate RR MS
  • Natalizumab if more active RR MS
  • Interferon B for primary and secondary progressive MS
  • Cannaboids effective in some
  • Metylprednisolone IV for 3-5 days shortens acute relapses but use sparingly (only for attacks lasting >24 hrs and moderate- severe), doesn’t alter overall progress
  • Baclofen/ gabapentin/ benzos for spasticity
  • Botulinum toxin injections for tremors
  • Self catheterisation if retainer
  • Amantadine, CBT and exercise can help with the fatigue
  • gabapentin for oscillopsia
  • exercise, cbt then amantadine for chronic fatigue
96
Q

Describe the clinical features of dementia? (6)

A
  • Memory deficit: struggle to learn new information and short term memory loss
  • Behavioural: altered personality, disinhibition, labile emotions, wandering
  • Physical: incontinence, reduced oral intake, difficulty swallowing
  • Language disorder: anomic aphasia, difficulty understanding language
  • Visuospatial disorder: unable to identify visual and spatial relationships between objects
  • Apraxia: difficulty with motor planning resulting in inability to perform learned purposeful movements
97
Q

What are the 4 main types of dementia?

A
  • alzheimers
  • vascular: stepwise decline, due to many small strokes
  • lewy body dementia: fluctuating cognitive impairment + parkinsons signs
  • frontotemporal dementia: social and behaviour changes are prominent
98
Q

What causes alzheimers dementia?

A

accumulation of B amyloid peptide resulting in neurofibrillary tangles, amyloid plaques, loss of Ach and progressive neuronal damage. Neuronal loss is quite selective to the hippocampus, amygdala, temporal neocortex and subcortical nuclei

99
Q

Give 3 RFs for alzheimers dementia

A

1st degree relative with AD, downs, ApoE E4 allele, vascular risk factors, depression (esp when combined with depression), low physical and cognitive activity, smoking

100
Q

What is the prognosis for alzheimers?

A

mean survival from diagnosis is 7 yrs- inability to self care eventually leads to poor nutrition, falls, dehydration which predispose to infections etc- esp pneumonia

101
Q

give 5 organic causes of dementia

A
  • depression
  • repeated head trauma
  • vitamin deficiency
  • alcohol
  • thyroid disease
  • huntingdons
  • parkinsons
  • CJD
  • wimples disease
102
Q

Describe the investigations for dementia

A
  • MMSE/ GPCOG
  • Bloods for reversible causes: B12, TFTs, toxicology
  • CT head: ventricle dilation and generalised hypertrophy
  • MRI head: hippocampal atrophy
103
Q

Describe the non pharmacological management of dementia

A
  • Avoid drugs that impair cognition: antipsychotics, sedatives, tricyclics
  • Aromatherapy, massage, multisensory stimulation, music, animal therapy for agitation
  • Memory aids such as orientation boards, rememberance therapy and life stories
  • Social care: risk assessments, care needs, mental capacity act
  • Depression: CBT, SSRI (citalopram), mirtazapine if severe
  • BP control
104
Q

Describe the pharmacological management of dementia

A
  • anticholinesterase inhibitors: eg rivastigmine, if mod- severe, can lead to peptic ulcers and heart block- not in vascular dementia
  • anti glutamatergic treatment: memantine, effective in late stage AD when AchE inhibitors not tolerated
  • antipsychotics: is severe psychosis/ agitation, not in lewy body dementia
  • vitamin supplements: Vit E shown to have some benefit in slowing decline
105
Q

How does a polyneuropathy present? and how are they classified?

A
  • motor and sensory disorder of multiple peripheral or cranial nerves
  • usually symmetrical
  • worse distally (glove and stocking/ distal weakness)
  • classified by acute vs chronic, functional (autonomic, motor, sensory, mixed) or by pathology (demyelination, axonal demyelination, both)
106
Q

Give 2 examples of polyneuropathies and their classifications

A
  • guillian barre- acute predominently motors, demyelinating

- alcohol abuse- chronic, initially sensory then mixed, axonal neuropathy

107
Q

How should a polyneuropathy be investigated?

A
  • FBC (polycythaemia), glucose, u&e (renal failure can cause), lft, tft (hypothyroid can cause), haematinics (b12 or folate deficiency) elecrophoresis (myeloma), ANA, ANCA (PAN, GPA, RA, SLE can cause), bone profile (sacroid- increases ca)
  • HIV test, leprosy test, sphyillis and lyme tests
  • cxr
  • urinalysis
  • consider LP
  • genetic tests
  • lead level (causes motor polyn)
  • antigalglycoside antibodies (autoimmune causes in GBS)
  • nerve conduction studies (axonal vs demyelinating)
108
Q

Give 3 causes of sensory neuropathy

A
  • Diabetes
  • CKD
  • leprosy
  • alcohol
  • B12 deficiency
  • GBS (will have motor also)
  • chemo drugs (vincristine, cisplatin, isoniazid)
  • nitrofurantoin, phenytoin and metronidazole can also cause
109
Q

Give 3 causes of motor neuropathy

A
  • guillian barre (usually mixed)
  • lead poisioning
  • charcot marie tooth
110
Q

Give 3 causes of autonomic neuropathy

A
  • DM
  • amyloidosis
  • guilliane barre
  • HIV
  • leprosy
  • sle
  • toxic
  • genetic
  • paraneoplastic
  • lambert- eaton myasthenic syndrome
  • If purely autonomic: primary automonic failure- causes inc multiple systems atrophy and parkinsons
111
Q

How is a polyneuropathy managed?

A
  • treat cause
  • usually involved PT, OT, foot care, shoe choice
  • avoid trauma
  • splinting
  • IV Ig for many demyelinating disease
  • steroids and immunosuppression for vasculitis
  • treatment of neuropathic pain
112
Q

What is cervical spondylosis and how does it present?

A
  • age related degeneration of annulus fibrosis + osteophytes + thickened ligamentum flavum = narrow canal and foramen = cord compression when neck flexes
  • limited, painful movement of neck, neck flexion produces tingling down arms- could be cords or roots
  • radiculopathy (roots impinged)- LMN signs and shooting pain and numbness at level of compression only
  • Cord compression- progressive symptoms, UMN signs and weakness below level of lesion, hoffman sign: involuntary thumb/ index finger movement when flick middle finger nail down)
113
Q

How is cervical spondylosis managed?

A
  • urgent MRI and refferal
  • analgesia
  • encourage gentle activity
  • injections
  • surgery (discectomy, laminectomy, collars)
114
Q

What is bells palsy and how does it present?

A
  • idiopathic facial nerve palsy
  • abrupt onset
  • complete unilateral facial weakness within 24-72 hrs, numbness or pain around ear, decreased taste sensation (ant 2/3 tongue), hyperacousis (N. to stapedius palsy), unable to wrinkle forehead (confirmed LMN), unilateral mouth sagging, drooling, speech difficulty, failure of eyelid closure leads to watering, redness and injury
115
Q

What could cause a facial nerve palsy (ie not bells)?

Think about other causes esp when bilateral, rashes, UMN signs, other CN involvement of limb weakness

A

stroke, brain stem tumour, MS ramsay hunt syndrome, lyme disease (common 1st presentation- always do bordella antibodies), meningitis, TB, acoustic neuroma, meningioma (cerebellopotine) , DM, sarcoid, guillian barre, skull base trauma, salivary gland or middle ear pathology (it runs through these)

116
Q

how should bells palsy be investigated?

A

To rule out other causes: FBC, ESR, glucose borrelia antibodies (for lyme), VSV antibodies (for ramsay hunt), CT/ MRI for SOL, stroke, MS, CSF sometimes for infections

117
Q

what is prognosis like for bells palsy? give one complication

A

incomplete paralysis recovers in a few weeks, 80% complete paralysis recovers fully, can be complicated by aberrant connection formation leading to crocodile tears (synkinesis- when eating stimulations crying not salivation)

118
Q

How is bells palsy managed?

A
  • Prednisolone if given within 72 hrs speeds recovery
  • antivirals don’t help.
  • Dark glasses
  • artificial tears, manual blinking, tape for sleep and surgery if long term is used to protect eyes when lid closure not possible
  • Doxycyline if lyme disease
119
Q

What are the key features of horners syndrome?

A

Meiosis + partial ptosis + apparent enopthalmos (sunken eye) + anhidrosis

120
Q

Describe where lesions can be to cause horners syndrome and what might occur there

A

May be at brainstem (demyelination, vascular disease) at cord (syringomelia), thoracic outlet (pancose tumour) on way up internal carotid (aneurysm) or orbit.
2 important causes:
- pancoast tumour
- carotic artery dissection: after severe whiplash or prolonged neck extension, MRA and CTangio to diagnose

121
Q

Describe the clinical features you might expect with cerebellopontine angle lesions

A
  • Unilateral conductive hearing loss (CN VIII)
  • Bells palsies (as hits CN VII)
  • Loss of sensation to face and corneal reflex (as hits CN V)
  • Speech impediments (CNIX, X)
  • Disequilibrium and ataxia and tremors (CN VIII, cerebellum)
  • Loss of motor control (medullary pyramids)
  • Hydrocephalus
122
Q

What may cause a cerebellopontine lesion

A
  • acoutic neuroma/ vestibular swchannoma
  • meningioma
  • aneurysm
123
Q

what is subacute combined degeneration of the spinal cord? (and what causes it)

A

Degeneration due to patchy loss of myelin in the dorsal column and lateral corticospinal tract of the cord. Spinothalamic tract usually preserved so pain and temp sensation in tact.
DUE TO B12 deficiency- this may be secondary to nitrous oxide abuse, alcoholism, veganism, pernicious anaemia, gastritis, ileal resections or copper and vit E deficiency can cause it

124
Q

Describe the clinical features of subacute combined degeneration of the spinal cord

A
  • Subacute, bilateral, symmetrical onset, usually only affecting a few levels of the cord
  • Numbness with loss of pressure, vibration and proprioception sensation, may get tingling sensation
  • Often proprioception is lost first so presents with ataxia (+ve rombergs test)
  • It then progresses to spastic weakness of arms, legs and trunk, classically with upgoing planters (UMN sign) but absent/ reduced knee and ankle jerks (LMN sign)- this is due to a combined peripheral neuropathy
  • Visual impairment and change in mental state may also be present
  • Symptoms of pernicious anaemia are often present but not always
125
Q

How is subacute combined degeneration of the cord diagnosed?

A
  • low B12 levels
  • MRI T2- increased signal within white matter of spinal cord predominantly in dorsal columns
  • Will get partial- full recovery when given B12
126
Q

Describe and explain the clinical features you may expect with a cavernous sinus syndrome

A
  • CN III down and out pupil, fixed and dilated
  • Trochlear loss of superior oblique
  • Abducens nerve loss of lateral rectus
  • All= opthalmoplegia + fixed, dilated pupil
  • V1 and V2 loss of sensation to forehead and cheeks
  • Optic chiasm tunnel vision
  • Internal carotid supplies optic nerve blindness
127
Q

What may cause a cavernous sinus syndrome?

A
  • Internal carotid aneurysms/ rupture
  • Venous sinus thrombosis
  • Pituitary adenoma
  • Meningioma
  • Carotid- cavernous fistula
128
Q

What causes wernickes encephalopathy and what are the classical features?

A
  • Due to thiamine (vit B1) deficiency- often seen in alcoholics
  • Triad of opthalomoplegia, ataxia and confusion (all three only seen in 10%)
  • Bilateral lateral rectus plasy and lateral nystagmus usually seen first, pupillary changes, papilodema and impaired vision can also be seen
  • Ataxia is due to cerebellum involvement- other signs may be present
  • Confusion is linked with memory impairment, amnesia, depression, psychosis, hypothermia
129
Q

How is wernickes encephalopathy treated?

A

give thiamine supplements (IV pabrinex)

130
Q

what is an argyll robertson pupil

A
  • Bilateral small pupils that still constriction on accommodation reflex but do not on light reflex
  • It’s a highly specific sign of neurospyhillis
  • Can also be a sign of diabetic neuropathy
131
Q

What causes creutzfeld jakob disease

A

Caused by prion proteins that cause misfolding of the proteins involved in the synapse. This leads to holes appearing the grey matter and a decline in cognitive function.
Prions may arise spontaneously, be inherited or be ingested (rare as have to eat cow brains).

132
Q

What is syringomyelia?

A

A tubular cavity in or close to the central canal of the cord. Takes out spinothalamic tract 1st usually usually bilateral loss of pain and temp sensation. They usually grow in the C spine and affect 20-30 yr olds.

133
Q

What can cause syringomyelia?

A
  • CSF blockage- Arnold chiari malformation (commonest), basilar invagination, masses eg cysts, tumours
  • After myelitis
  • After cord trauma
  • After rupture of an AV malformation
  • Fluid from neoplastic cells
  • Due to spinal tumours
134
Q

Describe the clinical features of syringomyelia

A
  • Pain and temp sensation loss with preserved prioprioception, vibration and light touch commonly over upper trunk, shoulders and arms
  • Dysaethesia (pain when touched) is common
  • LMN signs start as the syrinx extends and damaged the LMNs of the anterior horn cells
  • Syringobulbia: brain stem involved nystagmus, tongue atrophy, dysphagia, pharyngeal/ palatal weakness and Vth CN sensory loss
  • Charcot joints, scoliosis, painless hand ulcers are common
135
Q

How is syringomyelia manged?

A
  • MRI to confirm diagnosis, see size and if arnold chairi malformation
  • Decompression at foramen magnum for Arnold chairi malformations
  • Other surgeries may reduce pain and progression
  • Physio, analgesia
136
Q

Which bit of the cerebellum regulated what

A

Vermis (middle bit) regulates the trunk musculature (also get CN IV lesions, nystagmus) and hemispheres regulate the limbs (less marked nystagmus) . In general it is important for dampening stimulation to keep movements smooth.

137
Q

State and describe the 4 main causes of cerebellar pathology

A
  • Friedrich’s ataxia:
  • Strokes: posterior inferior cerebellar artery: often also has cranial nerve palsies, loss of consciousness (rare)
  • Tumours: meningioma, often cause hydrocephalus by obstructing 4th ventricle
  • Alcohol: long term abuse wernickes encephalopathy may also get opthalmoplegia and confusion
138
Q

What is friedrich’s ataxia?

A

Genetic condition causing frataxin defect. Symptoms start age 5-15 and get progressive loss of coordination and musle strength. Get cerebellar signs + heart problems (many get dilated cardiomyopathy), vision and hearing impairment, dorsal column degeneration (vibration and proprioception loss), muscle weakness in arms and legs with mixed UMN/ LMN - picture seen a lot in osces apparently

139
Q

What causes lyme disease

A
  • Caused by tick bite leading to infection with borrelia species
  • Commonest species in Europe is B. garnii
  • Which, left untreated leads to neuro complications in 10% after days- months
  • initially causes rash called erythema migrans (target like)
140
Q

Describe the neurological manifestations of lyme disease

A
  • uni or bilateral facial nerve palsies are commonest
  • meningism
  • mild encephalitis
  • peripheral mononeuropathies
141
Q

How is lyme disease managed

A

doxycyline for 2-3 weeks, complications need specialist management

142
Q

What is the role of IV dexamethasone 10mg QDS in meningitis management?

A
  • Especially helpful in pneumococcal meningitis
  • Pnemococcal meningitis: >60yrs, recent URTI, recent head surgery, skull# or CSF leak, immunocompromised
  • Given in all meningitis but stopped when causative organism determined not to be pneumococcal
  • Not given in meningococcal sepsis
143
Q

Describe the clinical features of GBS?

A
  • Symptoms evolve rapidly- over a few days/ week
  • lower limb and peripheral weakness and sensory symptoms often noticed first (often tingling initially)
  • loss of reflexes
  • Ascending weakness and LMN signs
  • Sensory loss may be in all modalities
  • Autonomic involvement later: erratic HR and BP, profound constipation/ diarrhoea, urinary retention progresing to incontinence, respiratory compromise
144
Q

how should GBS be investigated and diagnosed?

A
  • clinical diagnosis
  • Often raised protein in CSF
  • spirometry if resp compromise
  • SALT assessment for bulbar involvment causing unsafe swallow
  • monitor HR and BP, ECG if arrhythmias
  • nerve conduction studies abnormal in 80%
145
Q

Give 4 complications of GBS

A
  • resp failure (t2)
  • aspiration pneumonia
  • arrhythmias , BP fluctuations
  • chocking
  • DVT
  • urinary retention and constipation and incontience
  • limb contractures
  • dietary insufficiency
146
Q

How should GBS be managed?

A
  • admission
  • IVIG and plasmapheresis if: cant wakl >10m, severe autonomic features, swallow dysfunction, resp difficulties (reduced FVC/ reduction of >30% on lying flat)
  • STEROIDS DONT HELP
  • catheter, ng tube etc
  • monitor closely
  • senior review if deteriorates
147
Q

How should pseudo and true bulbar palsies be managed?

A
  • CT/ MRI
  • EMG
  • neuro refferal
  • admit if progressive or dysphagia
  • tx depends on cause
  • supportive: balcofen for spasticity and anticholinergics for drooling
  • salt refferal, dietician, pt/ot
148
Q

What are the 4 parkinons plus syndromes

A
  • Progressive supranuclear palsy (speech and swallow problems, early postural instability, verticle gaze palsies, little tremor)
  • Multiple systems atrophy (early autonomic features (PH, Incontincence), cerebellar signs, rigidty> tremor)
  • Corticobasal degeneration (apraxia, cortical sensory loss)
  • lewy body dementia (dementia preceeds/ predominates parkinsons, behavioural change)
149
Q

Describe the CFs of Myasthenia gravis?

A
  • WOMEN>men
  • MUSCLE WEAKNESS AND FATIGUABILITY (improves after rest)–> chewing harder at end of meal, symptoms worse in eve
  • EXACERBATING FACTORS: pregnancy, infection, low K+, climate change, emotion, exercise, drugs (bb, gent, opiates)
  • MUSCLES INVOLVED from commonest to rarest: EXTRAOCULAR (ptosis, diplopia), BULBAR (swallow, chew, speak) NECK (hard to lift head), PROXIMAL LIMB (lifting above head, standing from low chair/ bath), tunk (breathing), distal limb (grip)
150
Q

Give 6 tests (examination or otherwise) for MG?

A
  • LEVATOR TEST (ptosis gets worse when ask to sustain upward gaze)
  • COUNTING TO 50 (gets quieter and slurred over time)
  • EMG (decreased aplitude of muscle action potential w/ repition)
  • Achreceptor autoantibodies (50% w/ ocular involvement and 90% with generalised)
  • CXR/ CT shows enlarged thymus
  • Tensilon test (give tensilon (short acting ach esterase) and should see short term alleviation of symptoms, rarely done now as causes bradycardia which can be dangerous
151
Q

What is a myasthenic crisis and how is it managed?

A
  • SEVERE WEAKNESS of bulbar and chest muscles
  • often triggered bu something eg illness
  • manage w/ neostigmine, IVIG, plasmapheresis , pred and supportive care
  • ensure not a cholinergic crisis due to overteatment (which will present w similar symptoms but will get worse if you give neostigmine)
152
Q

Give 3 differentials for MG

A
  • Lambert eaton myasthenic syndrome (EMG amplitude improved w/ repitition, ocular involvement rarer, autonomic symptoms often)
  • Myopathies (ocular involvement rare)
  • MND (UMN features)
  • GBS (sensory symptoms often, acute onset, spreading)
    -MS (UMN only)
    -
153
Q

How is MG manged?

A
  • oral anticholinesterase inhibitors (pyridostigmine)- give propantheline if causes diarrhoea, other SEs = dry mouth, urinary retention, cholinergic crises
  • IV neostigmine, IVIG, plasmapheresis if crisis
  • immuno surpression for relapses (pred, aza)
  • thymectomy can cause remission or improvement in 60-80% even when no thyoma
154
Q

What is lambert eaton myasthenic syndrome, how does it present and how is it managed?

A
  • autoantibodies to NGCC in presynaptic membrane, mostly due to small cell cancer
  • gait difficulty early
  • eye signs
  • autonomic involvement (dry mouth, constipation, impotence)
  • hyporeflexia and weakness which improves after exercise
  • dipolpia and resp msucle involved if severe
  • treat w/ pyridostigmine IVIG and CXR/ CT follow up as symptoms may preceed cancer by up to 4 yrs
155
Q

What is huntingdons and what are the core features?

A
  • TAG repeats leading to degeneration of cordate, nucleus putamen and striatum leading to hyperkinesia
  • core features inc dystonia, incoordination, cognitive decline, chorea (rapid involuntary jerky movements)
  • facial grimaces and cognitive decline are usually 1st symptoms and develop around middle age
156
Q

How is huntingdons mangaged?

A
  • no effective drug treatment
  • benzos good for chorea
  • SSR for depression and antipsychotics for psychosis
157
Q

Describe the clinical features of myopathies?

A
  • GRADUAL ONSET PROXIMAL MUSCLE WEAKNESS (distal in myotonic dystrophy) (climbing stairs, getting out bath etc)
  • presevred tendon reflexes
  • no fasiculation
  • rapid onset suggests drugs, metabolic or neuropathy
  • pain and tenderness may be present in inflammatory myopathies but if predominant feature then think PMR
  • pain on exercise suggests ischaemic myopathy or metabolic (mcardles)
158
Q

Give 2 inherited and 2 aquired causes for myopathies

A

INHERITED: bichemical defects (mcardles, malignant hyperthermia) or musclar dystrophies (duchennes, myotonic, beckers)
AQUIRED: inflammatory (inclusion body myositis, dermato or polymoysitis) or non inflam (statins, alcohol, thyrotoxicosis, corticosteroids)

159
Q

How should myopathies be investigated?

A
  • genetic test
  • EMG
  • ESR and CK
  • muscle biopsy
160
Q

Paediatric pt presents with cateracts, distal muscle wasting and weakness and a glum looking face (ptosis, facial weakness, frontal bossing). What do they have and how can it be managed?

A
  • MYOTONIC DYSTROPHY (autosomal dominant, myotonic contractions due to abnormal muscle fibres)
  • mexiletine may help w/ myotonic but most die in middle age from cario/ resp complications
161
Q

What is a neurocutaneous syndrome? name 3

A

Disorders leading to growth of tumours in the brain, spinal cord, skin, bones and viseral organs

  • NEUROFIBROMATOSIS (t1= cafe au lait spots, lich nodiles, axilla and ingunial freckles// t2= bilateral swchannoma)
  • TUBEROUS SCLEROSIS (shagreen patches, cortical tubers, epilepsy, ungal fibromas)
  • STURGE WEBER SYNDROME (seizures, port wine stain, haemangiomas)
  • VON HIPPEL LINDAU (phaemochoromocytoma, haemangioma in any organ, hepatic and liver cysts)
162
Q

Describe how GCS is calculated

A

Motor: obeys command= 6, movement to pain crossing midline (purposeful- localises to pain)= 5, non purposeful movement to pain (no crossing midline/ withdraws from pain)= 4, flexion to pain (decorticate)= 3, extension to pain (decerebrate)= 2, none=1
Verbal: orientated =5, confused= 4, words not making sense (inappropriate) =3, incomprehensible sounds= 2, none= 1
Eyes: spontaneous =4, to voice= 3, to pain= 2, none =1

Y4 Neuro and SS (6 decks)

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