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Y5 Nervous System > List I - Core Conditions > Flashcards

List I - Core Conditions Flashcards

1
Q

What is epilepsy?

A
  • Neurological disorder in which a person experiences recurring seizures
  • International League Against Epilepsy describes epilepsy as a disease of the brain defined by any of the following conditions:
  • At least 2 unprovoked seizures occurring more than 24 hrs apart
  • One unprovoked seizure and a probability of further seizures similar to the general recurrence risk (at least 60%) after two unprovoked seizures, occurring over the next 10 years
  • Diagnosis of an epilepsy syndrome
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2
Q

What is status epilepticus?

A
  • Medical emergency defined as recurring seizures without regaining consciousness in between or lasts > or = 30 mins
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3
Q

What are the causes of SE?

A
  • Preceding seizure disorder - unknown epilepsy, non-compliance with AED, superadded effects of alcohol
  • No previous seizures - eclampsia, trauma (haemorrhage causing ischaemia), infection (arborvirus, HIV, syphilis, meningitis, encephalitis, abscess), tumour, CVA, metabolic (sudden +/- Ca2+, renal failure with cephalosporin therapy, peritoneal dialysis), hypoxia, drugs (antidepressants, OD, alcohol), dementia
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4
Q

What are the presenting clinical features of SE?

A
  • Symptoms
  • Symptoms of seizures, explained further in epilepsy
  • PMH - pregnancy (eclampsia), previous seizures
  • Signs
  • Signs of seizures, explained further in epilepsy
  • Non convulsive status - more difficult to identify, confusion, impaired memory, , odd behaviour, derealisation, aggression, psychosis +/- abnormalities of eye movement, eyelid monoclonus, odd posture
  • Examination - check BP (eclampsia)
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5
Q

What are the appropriate blood investigations for a person with SE?

A
  • FBC
  • U and E’s
  • Ca2+
  • BM - glucose
  • Consider anticonvulsant levels, toxicology screen, CO level, blood cultures
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6
Q

What are the appropriate urine investigations for a person with SE?

A
  • Pregnancy test (eclampsia)

* Consider dipstick/MC and S

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7
Q

What radiological investigations can be considered for a person with SE?

A
  • Consider CT
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8
Q

What other investigations can be done for a person with SE?

A
  • ECG

* LP

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9
Q

What is the approach to the management of a person with SE?

A
  • A to E assessment
  • Call for senior help if >5 mins
  • Anesthetist if GCS < or = 8
  • Obstetrician if eclampsia 0-5 mins
  • A - start timing, open airway, recovery position/keep safe, remove poorly fitting false teeth, guedel/nasopharygeal airway +/- ET tube/suction
  • B - 15L O2
  • C - HR, BP, ECG, IV access blood after 3-4 mins (FBC, U and E’s, LFT’s, Ca2+, Mg2+, PO4, glucose, clotting screen, toxicology, anticonvulsant levels, cultures, VBG
  • D - GCS, BM, temperature
  • 100mL 20% dextrose IV stat if BM <3.5mmol/L or unknown
  • Thiamine 250 mg IVI over 10mins if alcoholism/malnourishment OR
  • Pabrinex 2 pairs IVI over 30 mins (if not already had during the admission)
  • E - 5-20 mins early status, ask ward staff/review history of admission, call senior, attach ECG telemetry
  • Give lorazepam 2-4mg slow IVI over 30s - 2mins into large vein (repeat at 10 mins if no effect) OR
  • If no IV access, diazepam 10 mg pr (repeat up to 30 mg if no effect) OR
  • 1mL buccal midazolam 10mg - beware of respiratory arrest at end of bolus - check ECG and have resus equipment ready as can cause low BP, low HR, heart block
  • 20-30 mins established status - call anaesthetist and senior
  • Phenytoin 15-18mg/kg IVI at 50 mg/min (if not already on it)
  • If taking phenytoin monitor ECG, BP, temperature, phenytoin 100mg/6-8 hrs IV as maintenance (check levels) OR
  • Phenobarbitol 10mg/kg IVI over 10 mins
  • > 30 mins - refractory status, general anaesthesia (thiopental/propofol/ventilation) on ITU/HDU - frequent EEG monitoring
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10
Q

What further therapy should be given to a person with SE?

A
  • Known epilepsy - once seizures are controlled, start/resume oral AED at usual doses if patient known to have epilepsy
  • Dexamethasone 10mg IV if cerebral oedema/vasculitis
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11
Q

What are the complications of SE?

A
  • Anoxia - permanent brain damage (50% risk if primary presentation of epilepsy
  • Death - increased risk with length of attack
  • Mortality - 10-20%
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12
Q

How can SE be prevented / reduced?

A
  • Good compliance with AED

* No excess alcohol

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13
Q

What is a seizure?

A
  • Transient episode of excessive neuronal activity in the brain apparent either to subject/observer (clinical grounds)
  • Convulsion - seizure with motor activity
  • Primary generalised - originate in both hemi-speheres
  • Partial/focal - originate in 1 hemi-sphere
  • Secondary - originate in 1 hemi-sphere, then spread to both
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14
Q

What is epilepsy?

A
  • Chronic brain disorder with > or = 2 (recurrent) uprovoked/spontaneous seizures (or abnormal EEG >2 wks after seizure)
  • Generalised
  • Idiopathic generalised epilepsy syndromes (benign familial neonatal convulsions, childhood absence epilepsy, juvenile absence epilepsy, juvenile myoclonic epilepsy)
  • Symptomatic generalised epilepsy syndromes (infantile spasms - West syndrome assoc. with tuberous sclerosis, Lennox-Gastaut syndrome, cerebral malformations, progressive myoclonic epilepsies - inborn errors of metabolism/neurodegenerative diseases)
  • Localised
  • Idiopathic partial epilepsy syndromes (benign childhood/rolandic epilepsy with centrotemporal spikes)
  • Symptomatic partial epilepsy syndromes (cortical dysgenesis, CNS infection, head injury, AV malformations, brain tumours)
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15
Q

What are the causes of epilepsy?

A
  • Unknown in 50-70% assumed genetic
  • Genetic - neurocutaneous syndromes, Down’s syndrome, Fragile X, neurodegenerative disorders, inborn errors of metabolism
  • Cortical dysgenesis, cerebral malformation, tumours, cerebral damage
  • Head injury, birth asphyxia, hypoxia ischaemic injury, intracranial infection (meningitis/encephalitis)
  • Triggers - sleep, alcohol, drugs/rapid withdrawal, excitment, menstruation, fever, hypoglycaemia, trauma, hypoxia
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16
Q

How common is epilepsy?

A
  • 1% population (5/1000 school children)

* Lifetime risk of a generalised seizure 2-3%, 50% risk of further seizure after 1 unprovoked seizure

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17
Q

What are the presenting features of an absence seizure?

A
  • Onset - abrupt onset and termination (sometimes precipitated by hyperventilation)
  • Transient LOC - no motor signs except eyelid flickering and minor change in muscle tone
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18
Q

What are the presenting features of myoclonic seizures?

A
  • Onset - brief on/off, often repetitive, jerking movements of limbs, trunk or neck
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19
Q

What are the presenting features of tonic seizures?

A
  • Generalized increased tone, may fall +/- injury do not breathe and become cyanosed
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20
Q

What are the presenting features of tonic-clonic seizures?

A
  • Onset - lasts a few minutes
  • Tonic phase - generalised increased tone
  • Clonic phase - jerking, irregular breathing, cyanosis persists, saliva accumulates in mouth, tongue biting, urinary incontinence
  • Followed by LOC or sleep (post ictal) for up to several hours
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21
Q

What are the presenting features of atonic seizures?

A
  • Often with myoclonic jerk followed by transient loss in muscle tone - sudden fall to floor/drop of head
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22
Q

What are the presenting features of simple partial seizures?

A
  • Consciousness retained - child is aware
  • Motor - Jacksonian march clonic movements travel proximally
  • Sensory - occipital - distorted vison. Parietal - contralateral dysaesthesia/altered body image
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23
Q

What are the presenting features of complex partial seizures (temporal lobe seizures)?

A
  • Altered consciousness - due to abnormal electrical discharge spreading from originating site
  • Onset - starts as simple then becomes generalised
  • Aura - reflects the site of origin, smell, taste, distortion of sound/shape
  • Automatism - walking in non-purposeful manner, lip-smacking, picking at clothes (temporal lobe - premotor cortex)
  • Deja-vu/Jamais-vu - intense feeling of having been/never been in same situation before
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24
Q

What are the presenting features of a generalised secondary seizure?

A
  • Focal seizure manifests clinically (or ictal EEG) followed by a generalised tonic clonic seizure
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25
Q

What are the differential diagnoses for epilepsy?

A
  • Children - reflex anoxic seizure, breath holding attack, tics/habitual spasm, pseudoseizures, sleep myoclonus (physiological)
  • Adults
  • Life threatening - low O2, low glucose, metabolic Na+ or Ca2+ disturbance, trauma, meningitis/encephalitis, malaria, RICP, CVA, drug OD (alcohol/illicit), HTN/eclampsia
  • Less serious - vasovagal syncope, Stokes-Adams attack, narcolepsy
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26
Q

What are the appropriate blood investigations for epilepsy?

A
  • FBC, CS
  • U and E, LFT, glucose, Ca2+, Mg2+, PO4, serum toxicology (paracetamol/salicylate)
  • Plasma amino acids (if metabolic cause suspected)
  • WCC enzymes, DNA analysis
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27
Q

What are the appropriate urine investigations for epilepsy?

A
  • Urine toxicology

* Amino acids if metabolic cause suspected

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28
Q

What are the appropriate radiological investigations for epilepsy?

A
  • CT/MRI head
  • Indications - partial seizures, intractable/difficult to control, focal neurological deficit, evidence of neurocutaneous syndrome/neurodegeneration, children <2 yrs with non-febrile convulsions
  • Types - MRI FLAIR (fluid attenuated inversion recovery- greater sensitivity in detecting small lesions - temporal lobe/subtle cortical dysgenesis, SPECT
  • Consider LP after CT
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29
Q

What are the appropriate special test investigations for epilepsy?

A
  • Ictal or ambulatory EEG (interictal EEGs normal in 50%)
  • Infantile spasm - hypsarrhythmia - chaotic pattern of large amplitude slow waves with spikes and sharp waves)
  • Absence seizure - generalized bilaterally synchronous 3/s - slow - spike wave discharges, complex partial/temporal lobe (temporal lobe discharges)
  • Telemetry - with simultaneous video recording during sleep esp. if standard EEG normal
  • Skin/muscle biopsy - if neurocutaneous suspected
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30
Q

What is the conservative approach to the management of epilepsy?

A
  • 1st seizure - as per status management ABC
  • Conservative
  • Patient/parent education - condition, discourage over protection, activity (swimming, bathing, cycling, climbing, TV, driving: ok if seizure free for at least 1 yr if nocturnal - must inform DVLA, discuss anti-epileptic (AED) warn SE
  • MDT - neurology (first fit clinic), specialist epilepsy nurse, school staff
  • Ketogenic (fat) diet if intractable epilepsy
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31
Q

What is the medical approach to the management of epilepsy?

A
  • Medical (after = or > 2 seizures
  • Choice factors - seizure type/frequency (carbamazepine can make absence/myoclonic worse), social/educational consequences of seizure, possible unwanted SE’s of AED’s - aiming for monotherapy at the lowest possible dose to control the seizures
  • Prophylactic AED’s
    1. Generalized epilepsy (tonic clonic, myoclonic, absence)
  • 1st line sodium valproate, 300mg/12 hr po (up to 2.5g max)
  • Ethosuximide (for absence only)
  • 2nd line lamotrigine 25 mg/24h po (up to 50-100mg/24 h po max)
  • Topiramate (for tonic clonic only)
  1. Localized epilepsy (focal)
    - 1st line carbamazepine 100mg/12 hr po (up to 1g max), sodium valproate
    - 2nd line lamotrigine, topiramate, levetiracetam, gabapentin, vigabatrin (good for tuberous sclerosis assoc. seizures)

AED side effects - all cause drowsiness and occasional skin rashes

  • Changing medications - start new drug and gradually increase dose while gradually decreasing dose of former drug over 6wks
  • Stopping medications - usually after 2 yrs seizure free, reduce dose by 10% every 2-4 weeks - advise not to drive for 6 months after withdrawal
  • Rescue therapy - rectal diazepam 10mg or buccal midazolam, if prolonged seizures
  • Others include phenytoin 150-300mg/24 hrs po - must monitor levels as narrow therapeutic range
  • ACTH for infantile spasms
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32
Q

What is the surgical approach to the management of epilepsy?

A

Focal seizures - confirmed by EEG/functional neuroimaging

  • Anterior temporal lobectomy of non-dominant hemisphere (for mesial temporal sclerosis) or hemispherectomy, hemisphereotomy (does not involve hemisphere removal or problems with shifts in space)
  • Benefits - cessation of seizures and AED’s

Other procedures - intractable epilepsy
* Vagal nerve stimulation - delivered externally via programmable stimulation of wire implanted around vagal nerve

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33
Q

What are the complications of epilepsy?

A
  • Behavioural/emotional difficulties
  • Learning difficulties
  • Low self esteem
  • Anxiety
  • Depression
  • Sudden unexpected death (nocturnal seizure induced apnoea)
  • Prolonged fits - hypoxia - brain damage
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34
Q

What are the side effects of sodium valproate?

A
  • Increased appetite, increased weight, alopecia, significant teratogenicity
  • Thrombocytopenia
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35
Q

What are the side effects of carbamazepine?

A
  • Neutropenia, low sodium, double vision, liver enzyme inducer (can interfere with Warfarin/COCP)
  • Agranulocytosis
  • Leucopenia
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36
Q

What are the side effects of ethosuximide?

A
  • Nausea and vomiting, irritability, night terrors
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37
Q

What are the side effects of lamotrigine?

A
  • Double vision, Stevens-Johnson syndrome
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38
Q

What are the side effects of phenytoin?

A
  • Gum hyperplasia, coarse facial features, ataxia, slurred speech, acne
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39
Q

What are the side effects of vigabatrin?

A
  • Restriction of visual fields, sedation
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40
Q

What are the side effects of benzodiazepines?

A
  • Sedation, tolerance to effect, increased secretions
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41
Q

Which CN’s pass through the cavernous sinus?

A
  • III, IV, Va and VI
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42
Q

Which CN’s carry parasympathetic fibres?

A
  • III, VII, IX, X
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43
Q

What is the function of CN I? Olfactory

A
  • Sensory - smell, originates in the olfactory receptors of the nose
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44
Q

What is the manifestation of CN lesions in the nose?

A
  • Bilateral anosmia - URTI, smoking, sinusitis, head injury (olfactory neurons sheared via ethmoidal cribiform plate)
  • Unilateral anosmia - meningitis, frontal lobe tumour (olfactory groove meningioma)
  • Olfactory hallucinations - temporal lobe epilepsy
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45
Q

What is the function of CNII? Optic

A
  • Sensory (originates in the retina) - vision

* Pupil reflex - direct/consensual (sensory)

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46
Q

What is the manifestation of CN lesions in the optic nerve?

A
  • Monocular blindness (1 eye/optic nerve) - MS, temporal arteritis, optic nerve compression, trauma, papilloedema
  • Bi-lateral blindness - methanol, tobacco, amblyopia, neurosyphilis
  • Bi-temporal hemianopia (optic chiasm) - pituitary adenoma, craniopharyngioma, internal carotid artery aneurysm, retinitis pigmentosa
  • Homonymous hemianopia (1/2 field loss on contralateral side in optic nerve/thalamic laternal geniculate nucleus/optic radiation: upper parietal, lower temporal/cortex): CVA, abscess, tumour (macula sparing: occipital cortex - separate blood supply from MCA)
  • Quadrantopia (optic radiation: superior fields - parietal, inferior fields - temporal)
  • Scotoma (small localised are of blindness): glacoma, MS, optic neuropathy, AMD (age related macular degeneration)
  • Papilloedema (swelling of the optic disc, blurring of the margins, absent venous pulsation)/enlarged blind spot (RICP): tumour, abscess, encephalitis, hydrocephalus/BIH, retro-orbital lesion (cavernous sinus thrombosis, ischaemia of posterior ciliary artery, GCA)
  • Visual inattention (parieto-occipital, non-dominant hemisphere)
  • Colour blindness - inherited (x-linked recessive), acquired (optic nerve disorders)
  • Optic atrophy (pale optic disc): glaucoma, optic neuritis, long standing papilloedema
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47
Q

Which conditions are associated with miosis (small pupils)?

A
  • Bilateral, small, fixed - Argyll Robertson pupil (syphilis - accommodating but unresponsive)
  • Bilateral pinpoint - drugs (morphine), pontine lesion
  • Horner’s syndrome (ptosis, enophthalmos, anhydrosis)
  • Brainstem demyelination, tumour, infarction (lateral medullary sydrome)
  • Cervical cord/T1 root lesion - synringomelia, cervical rib, bronchial Ca (pancoast tumour)
  • Neck - neck surgery, carotid artery dissection
  • Cluster headache
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48
Q

Which conditions are associated with mydriasis (large pupil)?

A
  • Unilateral dilated - Holmes-Adie pupil (slowly accommodating but unresponsive - associated with depressed ankle jerks)
  • Unilateral dilates and deviated down and out - Oculomotor nerve lesion - unresponsive and not accommodating - associated with ptosis, impaired eye movements
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49
Q

Which conditions are associated with loss of direct light reflex?

A
  • Consensual lost - optic nerve lesion (optic neuritis, retro-orbital tumour)
  • Consensual normal - oculomotor nerve lesion (without mydriasis - DM, temporal arteritis, syphilis, HTN, with mydriasis: posterior communicating artery aneurysm, midbrain CVA with contralateral hemiplegia, RICP
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50
Q

What is the function of CNIII? Occulomotor

A
  • Motor (originates in the midbrain) - eye movements (supplies superior/medial/inferior rectus, inferior oblique), levator palpebrae
  • Pupil reflex - direct/consensual (motor - via parasympathetic fibres
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51
Q

What is the function of CNIV? Trochlear

A
  • Motor (originates in the midbrain) - eye movements (supplies superior oblique) SO4
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52
Q

What is the manifestation of CN lesions in the trochlear nerve?

A
  • Rare on its own

* Diplopia - down and in/ocular torticolis (head tilting to compensate) - DM, head injury (orbital trauma)

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53
Q

What is the function of CN V? Trigeminal

A
  • Sensory - opthalmic (runs with CNIII), maxillary and mandibular divisions
  • Motor (nucleus in pons) - muscles of mastication (temporalis, pterygoids, masseter)
  • Corneal reflex (sensory - opthalmic division)
  • Jaw jerk reflex - motor
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54
Q

What is the manifestation of CN lesions in the trigeminal nerve?

A
  • Pain but no sensory loss - trigeminal neuralgia, HZV, nasopharygeal carcinoma, acoustic neuroma
  • Jaw jerk deviates to 1 side - towards lesion
  • Absent corneal reflex - LMN lesion of opthalmic division, acoustic neuroma, meningioma, cavernous sinus lesion
  • Brisk jaw jerk - bilateral UMN lesion above pons - motor neurone disease, MS, infarction, tumour
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55
Q

What is the function of CN VI? Abducens

A
  • Motor (originates in the pons) - eye movements (supplies lateral rectus) LR6
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56
Q

What is the manifestation of CN lesions in the abducens nerve?

A
  • Horizontal diplopia in abducting eye - MS, Wernicke’s encephalopathy, false localizing in RICP, pontine CVA (fixed small pupils +/- quadriparesis)
  • Nystagmus of contralateral eye and failed adduction of ipsilateral eye - called ophthalmoplegia - lesion of medial longitudinal fasiculus - MS (demyelination), brainstem infarction, tumour
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57
Q

What is the manifestation of CN lesions in all three III, IV, and VI?

A
  • Cavernous sinus pathology (plus lesion of ophthalmic division of V) - cavernous sinus thrombosis, pituitary adenoma, internal carotid artery aneurysm
  • Superior orbital fissure lesion - meningioma
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58
Q

What is the function of CN VII? Facial

A
  • Sensory - taste (chorda tympani: anterior 2/3 tongue), hearing (nerve to stapedius)
  • Motor - (originates in the pons): muscles of facial expression (branches - temporal, zygomatic, buccal, mandibular, cervical)
  • Corneal reflex
  • Motor - temporal branch
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59
Q

What is the manifestation of CN lesions in the facial nerve?

A
  • Impaired taste; hyperacusis; forehead sparring/can raise eyebrows but lower facial signs (UMN lesion as bilateral innnervation): CVA, tumour, MS (demyelination); whole side of face affected (LMN lesion)
  • Pons - infarction, tumour, demyelination
  • Cerebellar pontine angle - acoustic neuroma, meningioma
  • Facial canal - plus hyperacusis/impaired taste; Bells palsy (most common viral infection causing unilateral weakness and failure of eye to close - Bell’s sign: eye roll’s up when tries to close eye; HZV (Ramsay Hunt syndrome), basal skull fracture/tumour, poliomyelitis, Paget’s, otitis media
  • Parotid - malignant parotid tumours, mumps, sarcoidosis
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60
Q

What is the function of CN VIII? Vestibulor cochlear

A
  • Sensory - hearing (cochlear nerve from spiral organ of Orti), balance (vestibular fibres from semicircular canals)
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61
Q

What is the manifestation of CN lesions of the vestibulor cochlear nerve?

A
  • Conductive hearing loss (BC>AC, lateralises towards the lesion)
  • Sensorineural hearing loss (AC>BC but both reduced, lateralises away from lesion
  • Horizontal/rotatory nystagmus (vestibular lesion)
  • Brainstem - Wernicke’s encephalopathy, MS, infarction, drugs (phenytoin)
  • Cerebellum (usually horizontal - fast phase towards side of lesion): MS, tumour, infarction
  • Labyrinth (usually rotatory - fast phase away from side of lesion - Hallpike +ve): Meniere’s disease, vestibular neuronitis, benign positional vertigo
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62
Q

What can cause a lesion of all three of the following CN’s V, VI and VIII?

A
  • Acoustic neuroma
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63
Q

What is the function of CN IX? Glossopharyngeal

A
  • Sensory - taste (posterior 1/3 of tongue), pharyngeal sensation
  • Gag reflex - sensory
64
Q

What is the function of CN X? Vagus

A
  • Motor - X originates in medulla: pharynx/vocal cords (recurrent laryngeal nerve)
  • Gag reflex - motor
65
Q

What is the manifestation of CN lesions of the glossopharyngeal and vagus nerve?

A
  • Hoarse voice, dysphagia, dysphonia - recurrent larygeal nerve lesion
  • Deviated palatal arch/uvula away from lesion (X lesion)
  • Absent gag reflex (IX or X lesion)
  • Bilateral CVA
  • MND
  • Brainstem infarction (lateral medullary syndrome)
  • Diptheria
  • Jugular foramen lesion (nasopharyngeal carcinoma, globus tumour)
66
Q

What is the function of CN XI? Accessory

A
  • Motor (originates in the medulla) - trapezius, sternomastoid
67
Q

What is the manifestation of CN lesion of the accessory nerve?

A
  • Failure to shrug shoulders/turn head (rare)
  • Poliomyelitis
  • Syringomyelia
  • Tumour
  • CVA
  • Bulbar palsy
  • Trauma
  • TB
68
Q

What are the functions of CN XII? Hypoglossal

A
  • Motor (originates in the medulla) - muscles of the tongue
69
Q

What is the manifestation of CN lesion in the hypoglossal nerve?

A
  • Fasiculations/wasting/deviates towards lesion (LMN lesion)
  • Trauma
  • Brainstem lesion
  • Neck tumours
  • Small/conical tongue which is slow to move (UMN lesion)
  • Motor neurone disease
  • Bilateral CVA
70
Q

What are the differential diagnoses for a CN lesion?

A
  • General for any CN
  • DM
  • CVA
  • MS
  • Tumour
  • Sarcoidosis
  • Vasculitis
  • Non-CN
  • Myasthenia gravis
  • Muscular dystrophy
  • Myotonic dystrophy
  • Mononeuritis multplex
71
Q

What are the appropriate investigations for a CN lesion?

A
  • Special tests
  • Goldman test (II) - formal bowl perimeter test to map out visual fields (useful for scotomas/monitor progress)
  • Calorimetry (VIII) - instill water 7 degrees below body temperature into ear canal
  • Brainstem evoked auditory responses (VIII)
72
Q

What is a peripheral neuropathy?

A
  • Damaged peripheral nerve(s) causing signs of a LMN lesion
73
Q

What is a mononeuropathy?

A
  • 1 nerve lesion
74
Q

What is mononeuritis multiplex?

A
  • Multifocal neuropathy caused by systemic disorder
75
Q

What is polyneuropathy?

A
  • Generalised disorder of multiple peripheral nerves
  • Classifications of either:
  • Sensory, motor or mixed
  • Demyelinating (site of disease is myelin sheath) or axonal (site is axon)
76
Q

What are the causes of mononeuropathies?

A
  • Trauma
  • Entrapment
  • Damaged vasa nervosum (blood supply)
77
Q

What are the causes of mononeuritis multiplex (WARDS PLC)?

A
  • Wegner’s granulomatosis
  • AIDS/amyloidosis
  • RA
  • DM
  • Sarcoidosis
  • PAN
  • Leprosy
  • Carcinomatosis
78
Q

What are the causes of polyneuropathy?

A
  • Alcohol
  • Arthritis
  • B12 deficiency
  • Carcinoma/chronic renal failure
  • DM
  • Environmental toxins (arsenic/lead)
  • Familial (Charcot-Marie-Tooth disease)
  • Guillain-Barr syndrome
  • Hepatic failure
  • Iatrogenic
  • Infection (TB, Lyme disease, HIV, CMV, EBV) idiopathic
79
Q

How common are peripheral neuropathies?

A
  • 8% prevalence
  • M:F = 1:1
  • Idiopathic (40%)
  • 2nd to disease process (60%)
80
Q

What is the pathophysiology of an UMN lesion?

A
  • Inspection - no muscle wasting (only after prolonged disuse)
  • Facial weakness - sparing of upper facial muscles
  • Tone - increased
  • Clonus - present
  • Power - spasticity, extensors weaker than flexors in upper limb and vice versa
  • Reflexes - increased, extensor plantar response (upgoing - also if aged <18 months) absent abdominal reflexes
81
Q

What is the pathophysiology of an LMN lesion?

A
  • Inspection - Muscle wasting, fasiculations
  • Facial weakness - Total unilateral facial weakness
  • Tone - reduced
  • Clonus - absent
  • Power - weakness (flaccid paralysis)
  • Reflexes - absent or reduced
82
Q

What is the pathology of a mononeuritis multiplex?

A
  • Patchy/asymmetrical with pain/weakness/sensory loss in ‘glove and stocking’ pattern (lower>upper)
83
Q

What is the pathology of a polyneuropathy?

A
  • Bilateral/symmetrical involvement with distal numbness/weakness - progression - neuropathic ulceration/joint deformity of hands (claw hand) or feet (pes cavus)
  • Clinical - LMN signs, sometimes sensory ataxia (distal joint position sense lost), ‘glove and stocking’ pattern of impairment of pain/temp/touch
84
Q

What is the function of the median nerve (C6-T1)?

A
  • Sensory - radial 3 1/2 digits and associated palm and dorsal tips
  • Motor - thenar eminence LOAF muscles (lateral 2 lumbricles, opponens pollicis, abductor pollicis brevis, flexor pollicis brevis)
85
Q

How does a median nerve lesion manifest clinically C6-T1?

A
  • Aching pain and/or paraesthesia/sensory loss over radial 3 1/2 digits and associated palm and dorsal tips (worse at night or on exertion, relieved by shaking/dropping over edge of bed, may involve arm), thenar eminence wasting, weak thumb abduction and flexion (and flexion of index finger - anterior interosseus nerve)
  • Phalen’s test - upside prayer sign for 1 min elicits symptoms
  • Tinel’s test - taping wrist elicits symptoms
86
Q

What are the causes of a median nerve lesion?

A
  • Carpal tunnel syndrome - compression by pressure of flexor retinaculum: pregnancy, DM (nerve sensitive to pressure), RA, amyloidosis, acromegaly, hypothyroidism (myxoedema)
  • Laceration - local deformity (OA, fracture)
87
Q

What are the investigations for a median nerve lesion?

A
  • Bloods - BM, ESR, TFT

* Nerve conduction studies

88
Q

What is the appropriate management for a median nerve lesion?

A
  • Splinting in partial wrist extension especially at night
  • Local steroid injection
  • Surgical decompression - division of the flexor retinaculum
89
Q

What is the function of the ulnar nerve (C7-T1)?

A
  • Sensory - medial 1 1/2 digits and associated palm and dorsum
  • Motor - all intrinsic muscles of the hand (except LOAF) and flexor digitorum profundus
90
Q

How does an ulnar nerve lesion manifest clinically C7-T1?

A
  • Pain and/or paraesthesia/sensory loss over medial 1 1/2 digits and associated palm and dorsum (may radiate from elbow)
  • Wasting of hypothenar eminence/interossei/medial 2 lumbricals (claw hand - less so if lesion at elbow as flexor digitorum profundus also denervated and if not chronic), cannot make good luck sign, weak wrist flexion (medial) weak little finger abduction, weak flexion of the 4th and 5th DIP’s
  • Froment’s test - try to remove a piece of paper held between both thumbs and index fingers - thumb flexes to hold paper (as adductor pollicis is weak)
91
Q

What are the causes of an ulnar nerve lesion?

A
  • Elbow trauma - compression at the epicondylar groove or between 2 heads of the flexor carpi ulnaris
92
Q

What are the investigations and management of an ulnar nerve lesion?

A
  • Nerve conduction studies
  • Rest - avoid pressure on the nerve
  • Soft elbow splinting - elbow extended for 6 months
  • Surgical decompression
  • Medial epicondylectomy - effective in <50% of cases
  • Transposition - re-routing
93
Q

What is the function of the radial nerve (C5-T1)?

A
  • Sensory - dorsal lateral hand around the root of the thumb (anatomical snuff box)
  • Motor - wrist/finger extension
94
Q

How does a radial nerve lesion manifest clinically?

A
  • Acute wrist drop (when arm pronated and elbow flexed) +/- sensory loss over anatomical snuff box
95
Q

What are the causes of a radial nerve lesion?

A
  • Compression against the humerus - prolonged abnormal posture of upper arm e.g. draped over arm chair due to alcohol excess (Saturday night palsy) or fracture
  • Management - splinting or surgery
96
Q

What is the main functions of the brachial plexus (C5-T1)?

A
  • Sensory and motor fibres to supply the upper limb
97
Q

How can a brachial plexus nerve lesion manifest clinically?

A
  • Pain/paraesthesiae and weakness in arm in variable pattern depending on location on plexus
  • Erb’s palsy - loss of rotator cuff function (waiters tip) - neurosurgery and physiotherapy
  • Cervical rib (thoracic outlet obstruction) - progressive wasting/weakness of intrinsic hand muscles, sensory loss (usually ulnar) +/- Raynaud’s (hands above head exacerbates paraesthesiae/white fingers - x-ray will reveal cervical rib
  • Pancoast tumour - bronchogenic Ca at lung apex invading lower roots, progressive pain in arm, distal wasting/weakness, sensory loss (usually C7/8, T1), Horner’s syndrome involving preganglionic sympathetic fibres
  • Neuralgic amyotrophy (especially nerve to serratus anterior) severe pain in shoulder/arm, usually after immunisation/surgery, pericapsular wasting/weakness, winging of scapula - spontaneous recovery (if at all) in 18 months-2 yrs
98
Q

What are the causes of brachial plexus lesions?

A
  • Acute trauma - shoulder dystocia during vaginal delivery (avulses part/all of plexus, RTA especially motorcyclists
  • Radiotherapy - for malignancy (breast)
  • Others - prolonged wearing of heavy rucksack, cervical rib, neuralgic amyotrophy/brachial neuritis, thoracic outlet compression
99
Q

What are the main functions of the phrenic nerve (C3-C5)?

A
  • C3, C4, C5 keeps the diaphragm alive!

* Motor - lowers the diaphragm during inspiration

100
Q

How can a phrenic nerve lesion manifest clinically?

A
  • Orthopnoea (with raised hemidiaphragm on chest x-ray)
101
Q

What are the causes of a phrenic nerve lesion?

A
  • Lung cancer
  • Myeloma
  • Thymoma
  • Cervical spondylosis/trauma
  • Thoracic surgery
  • C3-C5 herpes simplex virus
  • TB
102
Q

What investigations can be done for a phrenic nerve lesion?

A
  • Chest x-ray - raised hemi-diaphragm
103
Q

What are the functions of the lateral cutaneous nerve of the thigh (L2-L3)?

A
  • Sensory - anterolateral aspect of the thigh
104
Q

How can a lateral cutaneous nerve lesion manifest clinically?

A
  • Anterolateral burning of thigh pain (associated with recent change in patient’s weight)
105
Q

What are the causes of a lateral cutaneous nerve lesion?

A
  • Meralgia paraesthetica - compression of the nerve under the inguinal ligament
106
Q

What are the main functions of the sciatic nerve (L4-S3)?

A
  • Sensory - below knee posteriorly (tibial branch) and laterally (lateral sural cutaneous nerve from common peroneal)
  • Motor - muscles of posterior compartment of thigh (hamstrings: semi-tendinosus, semi-membranosus, biceps femoris) and all muscles below knee (via branches)
107
Q

How can a sciatic nerve lesion manifest clinically?

A
  • Sensory loss below knee laterally (posteriorly is compensated for) unable to flex knee, foot drop
108
Q

What are the causes of a sciatic nerve lesion?

A
  • Pelvic tumours, pelvic/femoral fracture

* Investigations - electrodiagnostic studies - to distinguish foot drop from common peroneal nerve injury

109
Q

What are the main functions of the superficial (lateral) peroneal nerve (L4-S2)?

A
  • Sensory - skin on dorsum of foot (except lateral 5th digit - sural nerve/adjoining sides of 1st and 2nd digits - deep peroneal nerve)
  • Motor - lateral compartment muscles (peroneal longus/brevis), extensor hallucis longus
110
Q

How can a superficial (lateral) peroneal nerve lesion manifest clinically?

A
  • Sensory loss over dorsum of foot, foot drop, unable to dorsi-flex ankle (or extend big toe) or evert the foot
111
Q

What are the causes of a superficial (lateral) peroneal nerve lesion?

A
  • Trauma to knee (RTA)

* Pressure - sitting cross legged (as winds round fibula head), DM, immobility

112
Q

What are the investigations and management of a superficial (lateral) peroneal nerve lesion?

A
  • Investigations - electrodiagnostic studies - to distinguish foot drop from sciatic nerve injury
  • Management - rest, should spontaneously resolve (as pathologically just a neuropraxia - conduction block
  • Foot drop splint - during spontaneous recovery
113
Q

What are the main functions of a tibial nerve lesion (L4-S3)?

A
  • Sensory - heel/sole
  • Motor - posterior muscles of leg/knee joint
  • superficial- gastrocnemius, soleus, plantaris
  • deep- popliteus, flexor hallucis longus, flexor digitorum longus, tibialis posterior
114
Q

What is the clinical manifestation of a lesion of the tibial nerve?

A
  • Sensory loss of the sole

* Unable to stand on tip-toe (plantarflexion) or invert the foot or flex toes

115
Q

What are the polyneuropathies?

A
  • Guillian-Barr Syndrome

* Charcot-Marie-Tooth Disease

116
Q

What is Guillain-Barr syndrome?

A
  • Acute inflammatory demyelinating polyneuropathy occurring <1 month (chronic if >3months)
117
Q

What are the causes of Guillain-Barr?

A
  • Triggers - may have preceding infection (c. jejuni, mycoplasma, CMV, HIV, EBV), vaccines, surgery
  • Pathology - autoimmune process whereby Abs cause inflammatory demyelination/variable axonal damage - includes respiratory and bulbar centres (if ascends high enough)
118
Q

What is the clinical presentation of Guillain-Barr?

A
  • Progressive ascending symmetrical muscle weakness (may be preceded by minor sensory symptoms)
  • Postural BP drop/dysrhythmias (autonomic involvement), diplopia, drooling dysphagia (and nasal regurgitation), dysarthria, breathing difficulty, (affects proximal muscles), urinary hesitancy/rentition
  • Signs - flaccid paralysis of limbs, early tendon arreflexia, minor sensory deficits
119
Q

What investigations are required for suspected Guillain-Barr?

A
  • Bloods - autoAbs to gangliosides (25%)
  • CSF - high protein/normal WCC (albuminocytological dissociation)
  • Nerve conduction studies - confirm demyelinating neuropathy
120
Q

What is the management of a patient with Guillain-Barr syndrome?

A
  • Progressive phase - ICU monitoring (vital capacity, ECG), NG tube (if cannot swallow), artificial ventilation/tracheostomy, regular PT (prevent joint stiffness/contractures), heparin 5000 IU/12h SC (thromboprophylaxis)
  • Non-ambulant phase - plasma exchange or high dose IV Igs (usually 5 daily injections)
121
Q

What is the prognosis of a person with Guillain-Barr-Syndrome?

A
  • 85% make complete/near recovery (complete paralysis is still compatible with complete recovery
  • Mortality 10%
122
Q

What is Charcot-Marie-Tooth Disease?

A
  • Clinical and genetically heterogenous group of disorders (hereditary sensory and motor neuropathies)
123
Q

What is the cause of Charcot-Marie-Tooth-Disease?

A
  • CMTA1 gene (most commonly) by autosomal dominant inheritance
  • CMTA2 gene - later age of onset
124
Q

What is the clinical manifestation of Charcot-Marie Tooth?

A
  • Champagne bottle appearance - slowly progressive distal wasting/weakness (anterolateral muscle compartment of leg), foot drop, pes cavus
  • Signs - Absent tendon reflexes, mild sensory loss, palpably thickened peripheral nerves
125
Q

What investigations are required for Charcot-Marie-Tooth Disease?

A
  • DNA analysis
  • Nerve conduction studies -marked slowing of nerve conduction velocities
  • Biopsy - segmental demyelination and hypertrophy
126
Q

What is the management of a person with Charcot Marie Tooth?

A
  • Medical - if in pain, amytriptyline 10-25mg/24h nocte or gabapentin 300mg/24h day 1 (then 300mg/12h day 2, then 300mg/8h day 3, then up to max 3.6g/24h)
  • Surgical - nerve release if severe pain
127
Q

What is the prognosis of a person with Charcot Marie Tooth?

A
  • Variable - some are in a wheelchair by middle age, others are asymptomatic with normal life span
128
Q

What are the blood investigations for polyneuropathies?

A
  • FBC, ESR, B12, U and E, LFT, TFT, glucose, serum protein electrophoresis autoAbs
129
Q

What are the urine investigations for polyneuropathies?

A
  • MSU - dipstick, MC and S, vasculitis, glucose, porphyrins, Bence-Jones protein
130
Q

What are the radiological investigations for polyneuropathies?

A
  • Chest x-ray - sarcoidosis, carcinoma
131
Q

Which special tests can be done for polyneuropathies?

A
  • CSF - high protein (especially in inflammatory neuropathies)
  • Neurophysiology - nerve conduction studies and EMG
  • Nerve biopsy - when unknown cause (or to confirm vasculitis, leprosy, chronic inflammatory demyelinating polyneuropathy)
  • Bone marrow biopsy/skeletal survey - myeloma
132
Q

What is a subdural haematoma?

A
  • Collection of blood deep to the dural layer of the meninges
  • Blood is not within the substance of the brain and is therefore called an extrinsic lesion or extra-axial
  • Can be unilateral or bilateral
133
Q

What are the causes of a subdural haematoma?

A
  • Decelerating injuries (commonly)
  • Reduced ICP
  • Dural metastasis
134
Q

What are the risk factors for subdural haematoma?

A
  • Older age - brain atrophy makes bridging veins more vulnerable
  • Falls - epilepsy, alcoholism, anticoagulation therapy
135
Q

How common is subdural haematoma?

A
  • 30% of severe head injuries are subdural haematoma
136
Q

How can subdural haematoma be categorised?

A
  • Acute
  • Subacute
  • Chronic
137
Q

What are the features of an acute subdural haematoma?

A
  • Most often due to high impact trauma
  • CT imaging is first line and often shows a cresenteric collection, not limited to suture lines
  • Appears hyperdense (bright) in comparison to the brain tissue
  • Large acute subdural haematomas will push on the brain (mass effect) and cause midline shift or herniation
  • Small subdural haematomas can be observed conservatively
  • Surgical options include monitoring of intracranial pressure and decompressive craniectomy
138
Q

What are the features of a chronic subdural haematoma?

A
  • Collection of blood within the subdural space that has been present for weeks to months
  • Due to rupture of the small bridging veins within the subdural space rupture and cause slow bleeding
  • Elderly and alcoholic patients are particularly at risk due to brain atrophy and therefore have fragile or taut bridging veins
  • Typically presents as a several week to month progressive history of either confusion, reduced consciousness or neurological deficit
  • Infants also have fragile bridging veins and can rupture in shaken baby syndrome
  • CT shows crescenteric shape, not restricted by suture lines and compress the brain (mass effect)
  • In contrast to acute subdurals, chronic subdurals are hypodense (dark) compared to the substance of the brain
  • If incidental finding, small in size with no associated neurological deficit it can be managed conservatively with the hope it will resolve in time
  • If the patient is confused, neurological deficit or severe imaging findings then surgical decompression with burr holes may be indicated
139
Q

What are the possible presenting clinical features of a subdural haematoma?

A
  • Fluctuating conscious level (35% thought to be an evolving stroke)
  • Physical / intellectual slowing
  • Sleepy
  • Headache
  • Personality change
  • Unsteady

PMH

  • Decelerating head injury
  • Alcoholism +/-

DH
* Anticoagulants

Signs

  • RICP
  • Seizures
  • Localizing neurological signs (unequal pupils, hemiparesis) occur later up to 63 days after injury
140
Q

What are the differential diagnoses for subdural haematoma?

A
  • Other reasons for RICP
  • Primary/Secondary tumours
  • Head injury
  • Haemorrhage (extradural, subdural, subarachnoid, intracerebral, intraventricular)
  • Infection (meningitis, encephalitis, cerebral abscess)
  • Hydrocephalus
  • Cerebral oedema
  • Status epilepticus
  • CVA
  • Dementia
  • CNS masses
  • Drug OD
141
Q

What are the appropriate investigations for subdural haematoma?

A
  • CT/MRI head - subdural = sickle-shaped/cresenteric
  • Shows clot +/- midline shift (beware bilateral isodense clots), sickle-shaped collection of blood extends more length of brain than extradural
  • ECG - may indicate cause of fall - arrhythmia
142
Q

What is the approach to management of a patient with acute subdural haematoma?

A
  • A to E assessment
  • Request urgent head CT
  • Medically stabilise (correct BP, seizures, diazepam 10-20mg pr/IV)
  • Elevate head out of bed to 30-40 degrees
  • Liaise/transfer urgently to neurosurgical unit - mechanical ventilation (hyperventilate to maintain PaCO2 to 3.5kPa - causes cerebral vasocontriction to reduce ICP)
  • Mannitol 20% 1-2g/kg (5mL/kg) IV over 10-20 mins (effect after 20 mins, lasts 2-6 hrs - aim for osmolality c.300mosmol/kg)
  • Dexamethasone 10mg IV stat then 4 mg/6h IV/po (only treats cerebral oedema)
  • Surgical - fluid restrict (<1.5L/24h) - closely monitor, treat underlying cause
143
Q

What is the approach to the conservative management of a patient with subdural haematoma?

A
  • For chronic haemorrhages - dexamethasone 4mg/6 hrs po - monitor closely - surgery indicated if midline shift
144
Q

What is the approach to the surgical management of a patient with subdural haematoma?

A
  • Burr-hole operation - first line for irrigation/evacuation
  • Craniostomy - first line if haemorrhage has organised
  • Craniotomy - second line - then treat underlying cause
145
Q

What are the possible complications of subdural haematoma?

A
  • Risk of coning, pneumonia, ARDS (from prolonged intubation/ventilation)
146
Q

What is the prognosis of a patient with subdural haematoma?

A
  • 80% chronic cases have a good outcome
  • 80% acute cases die (due to underlying brain injury
  • Poor prognosis if bilateral extensor plantar response, extensor response to pain, coma
147
Q

What is an extradural haematoma?

A
  • Collection of blood that is between the skull and the dura

* Almost always caused by trauma, typically low impact trauma e.g. a blow to the head or a fall

148
Q

What are the common features of an extradural haematoma?

A
  • Collection of blood is often in the temporal region since the skull at the pterion overlies the middle meningeal artery and is therefore vulnerable to injury
  • Classical presentation is the patient who initially loses, briefly regains and then loses again consciousness after a low impact head injury (lucid interval)
  • Lucid interval is lost eventually due to the expanding haematoma and brain herniation
  • As the haematoma expands the uncus of the temporal lobe herniates around the tentorium cerebelli and the patient develops a fixed and dilated pupil to the compression of the parasympathetic fibers of the 3rd cranial nerve
149
Q

What are the imaging features of an extra-dural haematoma?

A
  • Appears as a biconvex (or lentiform), hyperdense collection around the surface of the brain
  • Limited by the suture lines of the skull
150
Q

What is the mechanism of an extra-dural haematoma?

A
  • Temporal/parietal bone # shears the middle meningeal artery (may also be due to dural sinus tear)
151
Q

What is the pathophysiology of extra-dural haematoma?

A
  • Blood accumulates between the bone and the dura matter
152
Q

What are the symptoms of an extra-dural haematoma?

A
  • RICP - headache, drowsy, confused, reduced GCS following lucid period (hrs-days) or failure to regain consciousness/improve following head injury, vomiting, fits, hemiparesis
  • HPC - trauma at the temple
153
Q

What are the signs of an extra-dural haematoma?

A
  • RICP - Cushing’s response - low HR, high BP
  • Cheyne-Stokes respiration (damaged respiratory centres - crescendo-decrescendo-deep then shallow-tachpnoea with apnoea)
  • Ipsilateral pupil constriction (initially) then dilation/fixed (later-bilateral)
  • Reduced acuity, peripheral visual field loss, papilloedema (unreliable -50%), brisk reflexes, extensor plantar response
154
Q

What are the differential diagnoses for extra-dural haematoma?

A
  • RICP - primary or secondary tumours, head injury, haemorrhage, (extradural, subdural, subarachnoid, intracerebral, intraventricular), infection (meningitis, encephalitis, cerebral abscess), hydrocephalus, cerebral oedema, status epilepticus
  • Lucid interval of extra-dural bleeds - epilepsy, carotid dissection, CO poisoning
155
Q

What are the approapriate investigations for an extra-dural haematoma?

A
  • Radiological - CT head - Extra-dural =lEmon shaped haematoma (shows up white) extending from coronal to lambdoid sutures
  • Skull x-ray - may show temporal skull #
156
Q

What is the management for an acute extra-dural haematoma?

A

A to E

  • Request urgent CT head
  • Medically stabilise (correct BP, seizures diazepam 10-20mg pr/IV)
  • Elevate head of bed to 30-40 degrees
  • Liase transfer urgently to neurosurgical unit - mechanical ventilation (hyperventilate to maintain PaCO2 to 3.5kPa - causes vasoconstriction to reduce ICP
  • Mannitol 20% 1-2g/kg (5mL/kg) IV over 10-20mins (effect after 20 mins, lasts 2-6 hrs - aim for serum osmolality c.300mosmol/kg)
  • Give dexamethasone 10 mg IV stat, then 4 mg/6 hrs IV/po (for cerebral oedema)
  • For surgery fluid restrict (<1.5l/24h)
  • Closely monitor and treat underlying cause

Surgical options include
* Burr-hole operation or craniotomy - clot evacuation/ligation of bleeding vessel (especially if midline shift >5mm or haematoma >25ml)

157
Q

What are the risks / complications of extra-dural haematoma?

A
  • Risk of pneumonia / ARDS (from prolonged intubation/ventilation)
  • Prognosis - excellent if diagnosis and operations early
  • Poor if pre-op coma, pupil abnormality, decerebrate rigidity

Y5 Nervous System (2 decks)

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