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Phase2a > NEURO > Flashcards

NEURO Flashcards

1
Q

what are the most common pathological processes affecting motor neurones the brainstem or spinal cord

A
  • MND
  • spinal muscular atrophy
    • poliomyelitis
  • spinal cord/brainstem compression
  • vascular disease
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2
Q

what are the most common pathological processes affecting spinal roots

A
  • prolapsed intervertebral disc
  • cervical or lumbar spondylitis
  • tumours
  • malignant infiltration
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3
Q

what are the most common pathological processes affecting peripheral nerves

A
  • axonal degeneration or demyelination

- symmetrical polyneuropathy - distal weakness in limbs

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4
Q

what are the most common pathological processes affecting neuromuscular junctions

A
  • myasthenia gravis
  • lambert eaton myasthenic syndrome
  • congenital
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5
Q

dexcribe the features of brown sequard syndrome

A
  • ipsilateral weakness below lesion - damage of ipsilateral corticospinal (motor)
  • ipsilateral DC proprioception loss below lesion - ascending tracts damaged before they decussate in brainstem
  • contralateral loss of pain (spinothalamic) and temperature below lesion (fibres crossed 1-2 vertebral levels above when they enter)
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6
Q

describe extradural haemorrhage

A
  • traumatic
  • fractured skull
  • bleeding from middle meningeal artery (lacteration by bone)
  • lucid period (improvement in condition before deterioration)
  • rapid rise in intercranial pressure
  • coning and death if not treat
  • also can be due to tear in dural venous sinus
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7
Q

what is the presentation of an extradural haemorrhage

A
  • lucid period
  • then decreasing glasgow coma scale due to increased intercranial pressure (motor response, verbal response, eye opening)
  • increasingly severe headache
  • vomiting
  • confusion
  • seizures and hemiparesis with brisk reflexes and up going planter
  • ipsilateral pupil dilation
  • coma deepens
  • bilateral limb weakness develops
  • breathing becomes deep and irregular (brainstem compression)
  • bradycardia and hypertension in late
  • death due to respiratory arrest
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8
Q

what are the differentials of a extradural haemorrhage

A
  • epilepsy
  • carotid dissection
  • CO poisoning
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9
Q

what are the tests for an extradural haemorrhage

A
  • CT shows haematoma often biconvex/lens shaped (more rounded compared to sickle shaped subdural haematoma as dura keeps it in place
  • xray - normal or fractured
  • LP contraindicated
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10
Q

what is the management of an extradural haemorrhage

A
  • stabilise and transfer for clot evacuation and ligation of the bleeding vessel
  • care of airway - intubation and ventilation
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11
Q

describe a subdural haemorrhage

A
  • bleeding from bridging veins
  • commonest in small brains, alcoholics, dementia
  • shaken babies
  • anticoagulants
  • low pressure so soons stops bleeding
  • days/weeks later haematoma starts to autolyse
  • increased oncotic and osmotic pressure draws water into haematoma
  • increasing ICP over several weeks
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12
Q

what is the presentation of a subdural haemorrhage

A
  • fluctuating consciousness and insidious physical or intellectual slowing
    -sleepy
  • headache
  • personality change
  • unsteadiness
    signs
  • inc ICP
  • seizures
  • localising neuro symptoms are late -e.g hemiparesis, unequal pupils
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13
Q

what are the differentials of a subdural haemorrhage

A
  • stroke
  • dementia
  • CNS masses
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14
Q

what are the tests for a subdural haemorrhage

A
  • CT/MRI - clot/midline shift, crescent shaped
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15
Q

what is the management of a subdural haemorrhage

A
  • reverse clot

- surgical management >10mm or midline shift >5mm need evacuating - craniotomy or burr hole washout

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16
Q

describe a SAH

A
  • berry aneurysm
  • circle of willis rupture
  • 9/100000 a year
  • 35-65
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17
Q

what is the presentation of a SAH

A
  • sudden onset severe headache - occipital
  • photophobia
  • reduced consciousness
  • “thunderclap headache”
  • vomiting
  • collapse
  • seizures
  • coma
  • preceding sentinel headache due to small warning leak
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18
Q

what are the causes of a SAH

A
  • Berry aneurysm rupture (80%) commonly at junction between posterior communicating + ICA or anterior communicating and ACA
  • arteriovenous malformations (15%)
  • encephalitis
  • vasculitis
  • tumour
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19
Q

what are the risk factors for a SAH

A
  • Previous SAH
  • smoking
  • alcohol
  • hypertension
  • bleeding disorders
  • SBE
  • family history
  • polycystic kidneys
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20
Q

what are the differentials of SAH

A
  • meningitis
  • migrane
  • intracerebral bleed
  • cortical vein thrombosis
  • benign thunderclap headache - triggered by Valsalva manoeuvre e.g cogh
  • dissection of carotid or vertebral artery
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21
Q

what are the tests for SAH

A
  • CT
  • LP if CT clear but history suggests SAH >12 hours after onset to allow breakdown of RBC so positive sample yellow - bilirubin
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22
Q

what is the management of SAH

A
  • rexamine often
  • maintain cerebral perfusion
  • Nimodipine - Ca2+ antagonist - reduces vasospasm
  • surgery - endovascular coiling vs surgical clipping
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23
Q

what are the complications of a SAH

A
  • rebleeding
  • cerebral ischaemia due to vasospasm
  • hydrocephalus due to blocked arachnoid granulations
  • hyponatraemia
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24
Q

what are the branches of the aortic arch

A
  1. brachiocephalic trunk - R common carotid and right subclavian
  2. left common carotid
  3. left subclavian
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25
Q

at what vertebral level does the common carotid bifurcate

A
  • C3-C4
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26
Q

What are the stages of the internal common carotid

A
  1. cervical
    - anterior and medial to jugular
  2. petrous
    - penetrates temporal bone and runs anteromedially in carotid canal
    - can cause dissections in small trauma
  3. cavernous
    - through cavernous sinus - haemorrhage in this artery can press structures in the cavernous sinus
    - pierces dura
  4. supraclinoid (intradural)
    - into anterior and middle cerebral arteries
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27
Q

what are the structures in the cavernous sinus

A 
Opthalmic
Trochlear
Oculomotor
Maxillary
Carotid 
Abducens
Trochlear
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28
Q

what are the branches of the internal common carotid at the circle of willis

A
  1. opthalmic - retina
  2. posterior communicating
  3. anterior choroidal - optic tract, internal capsule, cerebral peduncle
  4. superior hypophyseal - pituitary gland, hypothalamus, optic chiasm
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29
Q

what is the presentation of a brain tumour

A
  1. raised ICP (is compliant at first, as ICP rises the CSF is pushed out then exponential rise in ICP, then brain is pushed out through foramen magnum (uncal hernia))
    - headache - worse on waking from sleep in the morning, due to dysuria in night - more volume of fluid in body, increased by coughing, straining and bending forward ( in which case think colloid cyst —- cardinal physical sign of this is papilloema - venous blood draining out of retina cant get back into intracranial compartment causing optic nerve oedema, venous engorgement and retinal haemorrhage)
    - reduced consciousness
    - nausea and vomiting
  2. progressive neurological deficit - motor, sensory, speech (receptive/expresisve), deteriorating memory, personality change)
  3. epilepsy - recent onset

(LETHARGY/TIREDNESS)

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30
Q

describe the grading of astrocytic/gliomal tumours

A
  1. pilocytic - paediatric and benign
  2. benign - premalignant/diffuse -astrocytes express glial fibrillary acid protein - use to detect
  3. anaplastic astrocytoma
  4. glioblastoma multiforme (GBM) - most common. all gliomas will progress to GBM
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31
Q

what is the pathogenesis of an astrocytic tumour

A
  1. initial genetic error in glycolysis
  2. mutation of isocitrate dehydrogenase 1 (IDH1)
  3. excessive build up of 2- hydroxyglutarate
  4. triggers instability in glial cells - mitoses
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32
Q

what are the tests for an astrocytic tumour

A
  • IDH1 +ve
  • IDH1 -ve = worse prognosis in over 50’s
  • molecular genetics
  • H+E
  • grade - histology
  • CT
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33
Q

what is the treatment of a astrocytic tumour

A
  • resection +months
  • temozolomide adjuvant with RT - max possible dose
  • gene therapy
  • dexamethasone improves brain performance
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34
Q

describe the WHO performance status for cancer

A
  1. capable of light work
  2. self caring >50% of day
  3. self caring <50% of day
  4. bed bound
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35
Q

a deletion of which gene is found in oligodendroglioma

A
  • 1P19q
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36
Q

what are the symptoms of meningitis

A 
early 
-headache
-fever
- leg pains
- cold hands and feet
- abnormal skin colour
later 
meningism 
- decreasing GCS 
- headache
- stiff neck 
- papilloedema 
- Kernigs sign - pain and resistance on passive knee extension with hip fully flexed 
- Brudzinski's sign
- petechial rash (non blanching) 
- signs of disease causing meningitis: zoster, cold sore/genital vesicles (HSV), HIV, parotid swelling (mumps), bleeding and red eye (leptospirosis
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37
Q

what are the differentials of meningitis

A
  • malaria
  • encephalitis
  • septicaemia
  • subarachnoid
  • tetanus
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38
Q

what are the tests for meningitis

A
  • cultures before LP
  • CT head
  • FBC, U+E, CRP, lactate, glucose
  • pneumococcal and meningococcal serum PCR
  • CXR
  • HIV test
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39
Q

what are the side effects of an LP

A
  • headache
  • paresthesia
  • CSF leak
  • damage to spinal cord
  • CNS herniation and death
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40
Q

which organisms are most likely to cause meningitis

A
  • Neisseria meningitidis - gram -ve diplococcus
  • Streptococcus pneumoniae - gram +ve diplococcus
  • haemophilus influenzae - gram -ve bacilli
    neonates
  • ecoli
    -group B strep - +ve cocci
  • listeria monocytogene in immunocompromised - gram +ve bacilli
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41
Q

what is the management of meningitis

A

GP/community - immediate IM benpen

hospital
- <55 cefotaxime
- amoxicillin+cefoxatime to cover for listeria >55, immunocompromised, alcohol misuse, pregnant
- dexamethasone + cefotaxime in confirmed pneumococcal/features of meningism
- consider vancomycin in return travellers
- prophylaxis of contacts - ciprofloxacin +rifampicin
( non needed in pneumococcal and Hib unless unvaccinated )

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42
Q

what are the signs of meningococcal sepsis

A
  • increased capillary refil time
  • cold hands and feet
  • hypotension
  • rash
  • limb/joint pain
  • tachycardia/hypnoea
  • rigor
  • death from CV failure as opposed to from increased ICP in meningitis
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43
Q

what are the symptoms of encephalitis

A
  • confusion
  • decreased GCS
  • coma
  • fever
  • headache
  • focal neurological signs
  • seizures
  • history of travel or animal bite
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44
Q

what are the causes of encephalitis

A
  • viral - HSV1+2, CMV, EBV, VZV (varicella zoster), HIV, measles, mumps, rabies
  • non viral - bacterial meningitis, TB, malaria, listeria, lymes disease, legionella
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45
Q

what are the investigations into encephalitis

A
  • bloods, culture, PCR
  • CT - bilateral temporal lobe involvement
  • LP - lymphocytosis, inc CSF protein, decreased glucose
  • EEG
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46
Q

what is the treatment of encephalitis

A
  • aciclovir IV
  • supportive
  • symptomatic treatment
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47
Q

what is the difference between missile and non missile head injuries

A
  • non missile = blunt
  • missile = penetration of skull or brain
    can be either focal or diffuse brain lesions
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48
Q

what is the difference between primary and secondary head injury

A

primary - immediate biophysical effects of trauma
secondary - physiological responses to trauma, effects of hypoxia/ischaemia, infection (present some time after traumatic events)

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49
Q

give examples of focal and diffuse non missile head injuries

A 
focal 
scalp 
- scalp contusions and laceration
skull 
-fracture - increased risk of haematoma, infection, aerocele. Flat surfaces cause linear fractures - can extend to skull base (contrecoup), angled or pointed objects cause open or depressed fractures 
meninges
- haemorrhage
- infection due to skull fracture 
brain 
- contusions
- lacerations
- haemorrhage
- infection 
- contact damage
- acceleration/deceleration injuries - traction on bridging veins causes subdural haemorrhage

diffuse
- axonal injury - a clinicopathological syndrome of widespread axonal damage including brainstem
-vascular - usually results in near immediate death, multiple petechial haemorrhages
- hypoxia/ischaemia - infarction and hypoxic ischaemic damage
- swelling - increased ICP caused by:
congestive brain swelling - vasodilation and inc cerebral blood volume
vasogenic oedema (extravasion of oedema fluid from damaged blood vessels)
cytotoxic oedema ( increased water content of neurones and glia)
- herniation due to bleeding and brain swelling

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50
Q

what is the difference between coup and contrecoup

A

coup - injury under site of impact

contrecoup - opposite side to where brain was hit

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51
Q

in which patients is brain infarction likely after a diffuse non missile brain injury

A

those who have had:

  • clinically evident hypoxia
  • hypotension with systolic BP <80 for >15 mins
  • inc ICP
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52
Q

what is chronic traumatic encephalopathy (cte) and its features

A
  • traumatic brain injury (TBI) with associated loss of conciousness
  • TBI risk factor for alzheimers disease
  • CTE often seen following repetitive mild traumatic brain injury
  • irribility, impulsivity, aggression, depression, memory loss
  • then dementia, gait and speech problems, parkinsonism
  • some have MND like symptoms
  • atrophy - neocortex, hippocampus, diencephalon, mamillary bodies
  • TDP 43 pathology in 85% (cardinal protein in dementia)
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53
Q

what is the pathology and epidemiology of multiple sclerosis (MS)

A
  • Inflammatory, demylinating disease
  • specific to NCS
  • 20-40 years
  • early course is relapsing/remitting
  • progressive disability over time
  • environment and genetics influenced
  • white males >coloured males
  • early onset age in women
  • age of exposure to certain environmental factors will decide whether someone will get MS
  • prevalance directly proportionate to distance from equator
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54
Q

how is MS classified

A
  • benign - little disability
  • relapsing/remitting - random attacks over a number of years, disability accumulates with each successive attack
  • chronic progressive - slow decline in neuro functions - primary (from disease onset) or secondary (following relapsing/remitting phase)
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55
Q

what environmental factors can contribute to MS

A
  • race
  • latitude increasing
  • age
  • diet
  • sanitation
  • socioeconomic status
  • multiple gene loci
  • climate
  • mutation
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56
Q

what is the pathology of MS

A
  • genetics and environment triggers
  • activated auto-reactive T cells
  • causes complete inflammatory attack with demyelination
  • oligodendrocyte loss
  • hypercellular plaque edge due to infiltration of tissue with inflammatory cells
  • extensive BBB disruption
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57
Q

what are the symptoms and signs of MS

A
  • optic neuritis - impaired vision and eye pain
  • spacisity
  • sensory - pins and needles, decreased vibration sense, trigeminal neuralgia, dysasthesia (unpleasant sensation when touched)
  • Lhermittes sign - electrical sensation running down back into limbs
  • nystagmus ( involuntary eye movement), double vision, vertigo, bladder and sexual dysfunction
  • uthoff’s - worse after a hot bath

atypical

  • aphasia
  • hemianopia
  • muscle wasting and fasciculation

first symptoms

  • weakness
  • paraesthesia (pins and needles)
  • visual loss
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58
Q

what can confirm diagnosis of MS

A
  • two or more CNS lesions disseminated in time and space (MRI)
  • exclusion of conditions giving a similar clinical picture
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59
Q

what are the tests for MS

A
  • MRI - sensitive but not specific for plaque detection and to exclude other causes e.g cord compression
  • CSF - oligoclonal IgG banding on electrophoresis suggests CNS inflammation
  • delayed visual, auditory and somatosensory evoked potentials
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60
Q

what are the differentials of MS

A
  • SLE
  • Sjogrens
  • acute disseminated encephalomyelitis
  • lymes disease
  • syphilis
  • AIDS
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61
Q

what is the management of MS

A

lifestyle - regular exercise, stopping smoking, avoid stress

disease modifying drugs :

  • dimethylfumarate for mild/moderate relapsing/remitting
  • monoclonal antibodies - alemtuzumat ( acts against T cells) and natalizumab (acts against VLA-4 receptors that allow immune cells to cross BBB)
  • interferon Beta/betaferon (1ST LINE)

treating relapses - methylprednisolone

symptom control

  • spasticity - baclofen or gabapentin
  • tremor - botulinum toxin
  • urgency/frequency - self catheterisation
  • fatigue - CBT and exercise
  • depression - amitriptyline
  • anxiety - alprazolam or diazepam
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62
Q

what are the differentials of epilepsy

A
  • postural syncope
  • hypoglycaemia
  • dystonia
  • TIA
  • migrane
  • hyperventilation
  • parasomnia
  • cardiogenic syncope
  • non epileptic seizure
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63
Q

what are the main causes of “blackouts”

A
  • problem with blood circulation (syncope) - low BP or due to heart
  • disturbance of brain function - either stress or epileptic seizures
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64
Q

define epilepsy

A

recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of brain, manifesting as seizures

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65
Q

what are the features of an epileptic seizure

A
  • 30-120 seconds
  • positive ictal symptoms
  • post ictal symptoms - headache, confusion or myalgia. temporary weakness or dysphagia
  • preceeding prodrome - change in mood or behaviour
  • may occour from sleep
  • may be associated with other brain dysfunction
  • typical seizure phenomena - deva ju, flashing lights, lateral tongue bite
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66
Q

what are the causes of epilepsy

A
  • 2/3 idiopathic
  • cortical scarring
  • developmental
  • space occupying lesion
  • stroke
  • vascular malformations
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67
Q

how is epilepsy diagnosed

A

by the history

  • tongue biting?
  • slow recovery?
  • deja vu?
  • fear?
  • triggers ( alcohol, stress, flickering lights?)
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68
Q

distinguish between focal, generalised and acute/provoked seizures

A

focal

  • one hemisphere
  • often seen in underlying structural disease

generalised
- rapidly engaging bilaterally distributed networks leading to simultaneous onset of widespread electrical discharge with no localising features referable to a single hemisphere <30 years

provoked/acute - not epilepsy

  • trauma
  • alcohol
  • raised ICP
  • haemorrhage
  • metabolic disturbance
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69
Q

what are the subtypes of focal epilepsy and what is the treatment

A
  • partial without impairment of consciousness
  • partial with impairment
  • secondary generalised - evolve to a bilateral convulsive seizure

treat with carbamazepine or Iamotrigine

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70
Q

what are the subtypes of generalised epilepsy and what is the treatment

A
  • absence seizures - breif 10 seconds pauses e.g in childhood
  • myoclonic seizures - suddent jerk of limb, face or trunk
  • tonic-clonic - loss of conciousness, limbs stiffen (tonic) then jerk (clonic)

treat with valproate or Iamotrigine

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71
Q

give some ways that antiepileptic drugs can work (AED’s)

A
  • inhibit Na channel reducing excitability and AP’s e.g carbamazepine
  • increase + channel - reducing excitability (k+ efflux)
  • inhibit SV2A - neurotransmiter not released
  • inhibit Ca2+ - neurotransmitter not drove to release e.g pregabalin and gabapentin
  • increase GABA receptor activity
  • inhibit GABA transaminase which degrades GABA
  • inhibit GABA transporter which degrades GABA
72
Q

what is the treatment of epilepsy

A
  • antiepileptic drugs
  • surgery (vagal nerve stimulator)
  • CBT
73
Q

what makes syncope different from epilepsy

A

it is situational

74
Q

give some features of non epileptic seizures

A
  • situational
  • psychiatric illness
  • rapid or slow recovery
  • ictal crying and speaking
  • eyes closed
  • prolonged atonia
75
Q

what are the signs/symptoms of parkinsons disease

A

ASYMMETRICAL FROM START

  1. Tremor (worse at REST) - not action tremor found in essential tremor or intention tremor found in cerebellar disease
  2. rigidity (hypertonia) - pain, problems with turning in bed
  3. bradykinesia - slowness to initiate movement, actions slow and decrease with amplitude with repetition. Gait = small steps, dragging one foot, writing smaller. reduced armswing, stooped posture

others

  • autonomic dysfunction - postural hypertension, constipation, urinary frequency, dribbling of saliva
  • sleep disturbance
  • reduced sense of smell
  • depression
  • dementia
76
Q

how is parkinsons disease diagnosed

A
  • by examination
  • resting tremor, asymmetrical
  • MRI to rule out other diagnoses
  • tone increased over entire radius of joint movement
  • bradykinesia
  • gait
77
Q

what is the pathology of parkinsons

A
  1. loss of dopaminergic neurones in the substantia nigra
  2. associated with lewy bodies/intracytoplasmic inclusion bodies in the basal ganglia, brain stem and cortex

most cases sporadic, though multiple genetic loci have been identified
mean onset age 60
causes reduced dopamine supply to striatum
1/2 cells died before symptoms

78
Q

what is the treatment of parkinsons

A
  • symptom control, not slowing disease progression
  • L dopa - dopamine - dopamine receptor
  • dopamine agonists -act on dopamine receptors e.g ropinirole
  • COMT/MAO-B inhibitors (enzyme inhibitors)
  • block DDC enzyme in periphery converting L-DOPA to dopamine allowing more L-dopa to cross BBB
  • block COMT enzyme in periphery breaking down L dopa
79
Q

what are the complications of parkinsons medication

A
  • wearing off
  • on dyskinesias - hyperkinetic movements when drugs work
  • off dyskinesias - painful dystonic posturing when drugs dont work
  • freezing
80
Q

what are the features of a 3rd nerve palsy

A
  • fixed dilated pupil
  • due to something pressing down on PSN
  • over apex of petrous part of temporal bone
  • downward and outward gaze
  • runs through cavernous sinus
81
Q

what are the four foramen of the ventricular system

A
  • foramen of luschka - lateral exit of 4th ventricle
  • foramen of magendie - medial exit of 4th
  • foramen of sylvius - third to fourth
  • foramen of munro - lateral to third
82
Q

which condition is a blockage of a foramen in the ventricles

A

obstructive hydrocephalus

83
Q

how is cerebellar syndrome diagnosed

A

ataxia on finger nose test

84
Q

give some disorders that can effect the brainstem

A
  • tumour - meningioma
  • inflammatory -MS
  • metabolic - central pontine myelonecrosis
  • trauma
  • spontaneous haemorrhage
  • infarction - vertebral artery dissection
  • infection - cerebellar abscess from ear
85
Q

what are the symptoms of brainstem death

A
  • pupils dont react to light
  • corneal reflex missing
  • cough and gag reflex missing
  • resp problems
  • response to pain missing
  • caloric vestibular reflex missing
86
Q

what are the symptoms of an upper motor neurone lesion

A
  • spasticity in stronger muscle groups (leg extensors and arm flexors) - increased tone that is velocity dependent - the faster you move the pts muscle the greater the resistance until it finally gives way (clasp knife)
  • hyperreflexia - reflexes are brisk
  • plantars upgoing (+ve babinski sign - when sole of foot stroked the big toe moves up and other toes fan out)
  • loss of skilled fine finger movements
87
Q

what are the symptoms of a lower motor neurone lesion

A
  • flaccidity/hypotonia
  • reflexes reduced or absent
  • plantars reamin flexor
  • wasting and fasciculation (twitching) of affected muscles
88
Q

what is a bitemporal hemianopia

A
  • half visual loss on opposite sides of visual fields due to pituitary tumour or internal carotid artery aneurysm
89
Q

what is a homonymous hemianopia

A
  • half visual loss contralateral to lesion in each eye dye to compression behind chiasm
  • stoke
  • tumour
90
Q

what can cause a CNVII lesion

A

LMN - bells palsy

UMN - forehead sparing, stroke, tumour

91
Q

wha can cause a CNVIII lesion

A

noise damage
pagets disease
herpes zoster

92
Q

which structures run through the carpal tunnel

A
  • median nerve
  • flexor digitorium superficialis tendons x4
  • flexor digitorium profundus tendons x4
  • flexor pollicis longus tendon x1
93
Q

what are the clinical features of carpal tunnel

A
  • aching pain in arm and hand - esp nocturnal
  • paraesthesia in thumb, index and middle fingers relieved by dangling hand over end of bed and shaking it “wake and shake”
  • may be sensory loss and weakness of abductor pollicus brevis and wasting of thenar eminence
  • light touch, 2 point discrimination and sweating may be impaired
94
Q

what are the causes of carpal tunnel

A
  • anything causing swelling or compression of tunnel
  • RA
  • amyloidosis
  • pregnancy
  • sarcoidosis
  • myeloma
  • local tumours
  • prolonged flexion
95
Q

what are the tests for carpal tunnel

A
  • neurophysiology to confirm lesions site and severity
  • maximal wrist flexion for 1 min may elicit symptoms
  • Tinels test - tapping over nerve at wrist can induce tingling
96
Q

what is the treatment of carpal tunnel

A
  • splinting
  • local steroid injection
  • decompression surgery
97
Q

what are the four main clinical patterns of motor neurone disease

A
  1. ALS/ amytrophic lateral sclerosis. - loss of motor neurones in motor cortex and anterior horn - combined UMN and LMN
  2. progressive bulbar palsy - CN IX-XII - problems with speech and swallowing, bulbar muscles first
  3. progressive musclar atrophy - anterior horn cell lesion - LMN only
  4. primary lateral sclerosis - loss of Betz cells in motor cortex - mainly UMN
98
Q

what is apraxia

A
  • consciously organised patterns of movements impaired e.g brushing teeth
99
Q

what is paresis

A

impaired motor function

100
Q

what is the epidemiology of MND

A

6/100000

MEN 3:2 WOMEN

101
Q

what is the presentation of MND

A
  • > 40
  • stumbling spastic gait
  • foot drop and proximal myopathy
  • weak grip and shoulder abduction
  • aspiration pneumonia
  • UMN + LMN signs
  • NO sensory loss or sphincter disturbance - outruling MS
  • never effects eye movements - distinguishing from myasthenia gravis

later

  • tongue wasting (bulbar)
  • phrenic nerves - diaphragm moves up - breathing main cause of death
102
Q

what are the tests for MND

A
  • neurophysiology - nerve conduction studies/electromyography - sensory normal, motor amplitude low
  • MRI head/spine
  • LP
103
Q

how is MND diagnosed

A

definite - LMN +UMN signs in 3 regions
probable - 2
probable - 1+lab

104
Q

what is the management of MND

A
  • MDT
  • riluzole - inhibits glutamate release - NMDA receptor antagonist can prolong survival
  • excess saliva - advice on positioning, oral care, suctioning, antimuscarinic
  • resp - NIV, BiPAP
  • dysphagia - blend food, gastrostomy option
  • spascity - exercise, orthotics
  • communication equipment
105
Q

how is dementia diagnosed

A
  • history
  • cognitive testing - AMST (abbreviated mental test score)
    6CIT
  • year?
  • month?
    -address (5parts)
    -20-1 count
  • reverse months of year
    -repeat address
106
Q

define dementia

A

a set of symptoms including memory loss, problem solving or language, that is gradual onset and progressive

107
Q

what are the main types of dementia

A
  • Alzheimers disease
  • vascular dementia
  • lewy body dementia
  • frontotemporal
108
Q

what are the tests for dementia

A
  • MRI can identify other pathologies
  • FDG, PET, SPECT - subtypes
  • EEG
109
Q

what are the symptoms of alzheimers disease

A
  • > 40
  • persistant, progressive and global cognitive impairment - visuospatial skill, memory, verbal abilities, planning
  • anosognodia - lack of insight into problems of disease - missed appointments, misunderstood conversation or plots of films, mishandling of money
  • irritibility
  • mood disturbance
  • aggressive
  • psychosis
  • agnosia (may not recognise self)
  • apathy
  • disengagement
110
Q

what is the cause of alzheimers disease

A
  • environment and genetics
  • accumulation of beta amyloid peptide, a degradation protein of amyloid precursor protein, results in progressive neuronal damage, neurofibrillary tangles, inc amyloid plaques, loss of Ach
111
Q

what are the risk factors for alzheimers

A
  • 1st degree relative
  • down’s syndrome
  • homozygosity for apolipoportein E E4 allele
  • vascular (hypertension, diabetes, AF)
  • Decreased physical or cognitive activity
  • depression
  • loneliness
  • smoking
112
Q

what are the differentials of alzheimers disease

A
  • vascular dementia
    subcortical frontal pattern (attention difficulties, motor/cognitive slowing and executive problems) and visuo-spatial difficulties
  • lewy body dementia
    fluctuating cognition, pronounced disturbances in attention and concentration, working memory and early visuoperceptual deficits, visual hallucinations and spontaneous parkinism
  • depressive pseudodementia
113
Q

what are the alzheimers diagnostic criteria 2014

A
  • presence of early and significant episodic memory impairment that includes:
  • gradual and progressive change in memory function over 6 months
  • amnestic syndrome of hippocampal type

-b in vivo evidence of alzheimers pathology e.g mutation present (e.g APP) increased tracer retention on amyloid PET

114
Q

what features of a history would EXCLUDE alzheimers

A
  • sudden onset
  • sudden gait/behavioural changes/seizures
  • early extrapyramidal signs
  • early hallucinations
  • cognitive fluctuations
  • focal neurological features
115
Q

what is the management of dementia

A
  • acetylcholinesterase inhibitors (AchE) - donepezil, rivastigmine and galantamine
  • antiglutamatergic treatment - NMDA antagonists such as memantine
  • antipsycotics
  • vitamin supplements
  • non cognitive symptoms may be helped by aromatheraphy, massage, animal assisted therapy
116
Q

what are the symptoms of depression

A
  • continuous low mood or sadness
  • feeling hopeless and helpless
  • low self asteem
  • tearful
  • guilt
  • irritable and intolerant of others
  • no motivation
  • difficulty making decisions
  • not getting enjoyment out of life
  • anxious
  • suicidal thoughts

physical

  • moving or speaking slower than usual
  • changes in appetite or weight
  • constipation
  • aches and pains
  • lack of energy
  • low sex drive
  • menstrual cycle changes
  • disturbed sleep

social

  • not doing well at work
  • avoiding friends and family
  • neglecting hobbies and interests
  • difficulties in home and family life
117
Q

what are the risk factors for depression

A
  • upsetting or stressful life event - bereavement, divorce, illness, redundancy
  • downward spiral of events
  • older
  • socioeconomic status
  • personality - low self esteem or self critical
  • family history
  • giving birth
  • loneliness
  • alcohol and drugs
  • illness
118
Q

how is depression diagnosed

A

5/9 with at least 1 core

CORE

  • during last month have you felt down, depressed or hopeless
  • do you have little interest or pleasure doing things

Other

  • fatigue
  • worthlessness/guilt
  • suicidal thoughts
  • diminished concentration
  • psychomotor agitation or retardation
  • insomnia/hypersomnia
  • significant appetite/weight loss
119
Q

list 2 questionnaires for depression

A

patient health questionnaire - PHQ9

generalised anxiety disorder assessment - GAD7

120
Q

what are the differentials of depression

A

Greif

  • retains capacity for pleasure
  • biological symptoms of loss of sleep, appetite and concentration
  • distress related to loss
  • in waves
  • able to look forward to future
  • cope without medical intervention
  • passive wish for life to end

dementia

substance abuse

hypothyroidism

121
Q

what is the management of depression

A

of suicide risk
-crisis resolution and home treatment team for urgent assessment

safeguarding

comorbidities

  • anxiety
  • alcohol
  • psychosis
  • eating disorders
  • dementia
psychological 
-referral or self referral to IAPT (improving access to physchological therapies)
---- low intensity 
individual self guided CBT
CCBT (computerised)
group physical activity
group peer support
---- high intensity 
group CBT 
individual CBT 
couples
----counselling

exercise

selective serotonin reuptake inhibitors (SSRI's) 
- fluoxetine (prozac)
- citalopram
- sertraline 
tricyclic antidepressants (TCA's)
- amitryptiline
122
Q

what is the structure of the cerebellar cortex

A
  • molecular layer
  • purkinje layer - cells in this layer (purkinje cells are only output)
  • mossy fibres
  • climbing fibres
123
Q

what are the symptoms + signs of cerebellar disease

A
  • loss of precision of fine movement/motor skills
  • unsteadiness when walking/worse in dark
  • stumbles and falls
  • slurred speech
  • swallowing difficulties
  • tremor

signs

  • nystagmus ( involuntary eye movement)
  • dysarthria ( unclear speech_
  • action tremor
  • dysdiadochokinaesia (cant perform rapid alternate movements)
  • truncal and limb ataxia
  • gait ataxia
124
Q

what is the SARA for ataxia

describe the grading and how it is decided

A

Scale for assessment and rating of ataxia
mild - mobilising independently or with one walking aid
moderate - 2 walking aids/ frame
severe - predominantly wheelchair dependent

  1. gait
  2. stance
  3. sitting
  4. speech
  5. finger chase
  6. nose finger test
  7. fast alternating hand movement
  8. heel shin slide
125
Q

what are the tests for cerebellar disease

A

MRI brain - cerebellar atrophy

excludes tumours, MS, cerebrovascular damage, hydrocephalus

126
Q

what is a peripheral neuropathy

A

any condition of peripheral nerves - acute or chronic

  • chronic divided into small and large fibre
  • large into axonal or demyelinating
127
Q

what do large and small nerves detect

A

large

  • proprioception
  • light touch
  • pressure
  • vibration

small

  • pain
  • warm
  • cold
128
Q

give an example of a mononeuropathy

A

carpal tunnel (median nerve) C6-T1

129
Q

what are the motor symptoms of peripheral neuropathy

A
  • muscle cramps
  • weakness
  • fasciculations
  • atrophy
  • pes cavus (high arched feet)
130
Q

what are the 3 categories of peripheral neuropathy

A 
symmetrical 
- length dependent 
-initially sensory --> then sensorimotor
asymmetrical sensory 
- patchy distribution of symptoms
-dorsal root ganglia are affected 
- paraneoplastic, sjogren, gluten sensitivity/CD
asymmetrical sensorimotor 
-mononeuritis multiplex
- vasculitis
131
Q

how is peripheral neuropathy diagnosed

A

examination

  • decreased or absent tendon reflexes
  • sensory deficit
  • weakness - muscle atrophies

neurophysiological
- nerve conduction studies - distinguish demyelinating from axonal

  • fbc
  • esr
  • glucose
  • U+E
  • LFT
  • B12
  • electrophoresis
  • ANA
  • ANCA
  • CXR
  • urinanalysis
  • LP
132
Q

what happens to nerve potentials in demyelinating and axonal peripheral neuropathies

A
  • demyelinating - slow conduction velocities

- axonal - reduced amplitudes of potentials

133
Q

what are the causes of peripheral neuropathies

A 
Diabetes
Alcohol 
Vitamin deficiency (B12)
Infective (TB)
Drugs
Hypothyroidism 
RA
connective tissue disease 
renal disease
paraneoplastic 
amyloidosis 
hepatitis
HIV
lyme
vasculitis
Charcot marie tooth (CMT) (inherited demyelinating)
134
Q

what is Guillain Barre syndrome

A

An acute inflammatory demyelinating polyneuropathy

  • rapid ascending paralysis and sensory deficits
  • muscle weakness, proximal more effected e.g trunk, respiratory
  • infection may preceed e.g campylobacter jejuni, CMV, zoster, HIV, EBV
  • tachycardia, sweating, arrhythmias
  • immediate plasma exchange needed (IVIg)
  • demyelinating/motor axonal/axonal sensorimotor
135
Q

what is the treatment of polyneuropathies

A 
symptomatic 
- pain (amitryptiline, gabapentin, pregabalin)
- cramps (quinine)
- balance (physio/aids)
treat cause
136
Q

what is myasthenia gravis

A

autoimmune disease mediated by autoantibodies to nicotinic acetylcholine receptors on post synaptic side of neuromuscular junction

137
Q

what is the presentation of myasthenia gravis

A
  • slowly increasing or relapsing muscular fatigue
  • muscle groups affected in order: extra ocular, bulbar, face, neck, limb girdle, trunk
    signs
  • ptosis (drooped upper eyelid)
  • diplopia (double vision)
  • myasthenic snarl
138
Q

what are the symptoms of myasthenia gravis exacerbated by

A
  • pregnancy
  • hypokalaemia
  • infection
  • overtreatment
  • emotion
  • exercise
  • gentamicin
  • opiates
  • tetracycline
  • quinine
  • BB’s
139
Q

what are the differentials of myasthenia gravis

A
  • polymyositis
  • SLE
  • botulism - botulinum toxin interferes with fusion of synaptic vesicles into synaptic cleft
  • Takayasu’s arteritis
140
Q

what are the associations of myasthenia gravis

A
  • AI especially RA and SLE
  • <50 female > male
    >50 male >female
141
Q

what are the tests for myasthenia gravis

A
  • increased anti AchR antibodies in 90%
  • if -ve look for MuSK antibodies (muscle specific tyrosine kinase)
  • EMG (electromyography) - decremental muscle response to repetitive nerve stimulation
  • imaging - CT to exclude thyoma
  • ptosis improved with ice application
142
Q

what is the treatment of myasthenia gravis

A
  • anticholinesterase e.g pyridostigmine
  • immunosuppression e.g prednisolone
  • osteoporosis prophylaxis - bisphosphonate
  • thymectomy - removal of thymus
143
Q

what is the difference between primary and secondary headaches

A

primary

  • migrane
  • cluster
  • tension

secondary

  • meningitis
  • SAH
  • GCA
  • idiopathic intercranial hypertension
  • medication overuse
144
Q

what is trigeminal neuralgia

A

face pains and headache caused by compression of the trigeminal nerve

145
Q

what are the red flags for secondary headache

A
  • > 50
  • Hx of HIV or cancer, trauma or risk factors
  • changing personality or cognitive dysfunction
  • vomiting

headache

  • jaw claudation or visual disturbance - GCA? amaurosis fugax also in TIA
  • changing in frequency, characteristics or associated symptoms
  • postural
  • sudden onset/thunderclap
  • exercise of valsalva
  • focal neurological symptoms

exam

  • fever
  • altered conciousness
  • neck stiffness (brudzinski’s sign) - severe neck stiffness causes the hips and knees to flex when the neck is flexed
  • others
146
Q

when should you immediately refer someone with a headache to a specialist

A
  • thunderclap headache - ? SAH
  • seizure and new headache
  • suspected meningitis
  • suspected encephalitis
  • red eye ? acute glaucoma
  • headache and new focal neurology including papilloedema
147
Q

what is the presentation of a migrane

A
  • with or without visual aura lasting 15-30 minutes preceeding headache
  • unilateral
  • throbbing pain
  • moderate/severe - lasting 4-72 hours
  • without aura can have nausea and vomiting with out without photophobia/phonophobia
  • may have allodynia - all stimuli produce pain
148
Q

describe the features of a migrane aura

A
  • visual: chaotic distorting, melting and jumbling of lines, dots or zigzags, hemianopia or scotomata
  • somatosensory: paraesthesiae spreading from fingers to face
  • motor: dysarthria (unclear articulation of speech) + ataxia, opthalmoplegia or hemiparesis
  • speech - dysphagia or paraphasia
149
Q

what can trigger a migrane

A 
Chocolate 
Hangover
Orgasm
Cheese
Oral contraceptive
Lie ins 
Alcohol
Travel
Exercise
150
Q

how is migrane diagnosed

A

-5 or more headaches
- 4-72 hours
- two of following:
unilateral
pulsing
aggravaton by physical activity
moderate/severe
- one of N+V or photo/phonophobia

151
Q

what are the differentials of a migrane

A
  • cluster/tension
  • cervical spondylosis
  • hypertension
  • intercranial pathlogy
  • sinusitis/otitis media
  • dental caries
152
Q

what is the management of migrane

A
  • avoid triggers

prophylaxis

  • propranolol 1st line (BB)
  • topiramate 2nd line (anticonvulsant)
  • riboflavin (B2)
  • amitriptyline (TCA)
  • botulinum toxin type A last resort for chronic migranes

during attack

  • triptan (CI in IHD, hypertension, SSRI’s)
  • NSAID/paracetamol
  • antiemetics

non pharmacological

  • warm/cold packs
  • rebreathing into paper bag to increase CO2
  • acupuncture
153
Q

how is a tension headache diagnosed

A
  1. 30 min - 7days
  2. pressing/tight band
    bilateral
    mild/moderate
    not aggravated by routine physical activity
  3. both of following:
    NO N+V
    1 of photo/phonophobia
154
Q

what is the presentation of a cluster headache

A
  • severe or very severe unilateral orbital, supraorbital and/or temporal pain lasting 15-180 minutes if untreated
  • accompanied by ipsilateral cranial autonomic features (watery/bloodshot eye, lid swelling, lacrimation, facial flushing, rhinorrhoea, miosis+/- ptosis) and or a sense of restlessness or agitation
  • frequency of 1 per day to 8 per day
  • P/P possible
  • cluster of 4-12 weeks
  • treat with 100% O2 for 15 min with non rebreather (not in COPD), SUMATRIPTAN AT ONSET
  • prevent with verapimil - CCB
  • at least 5 attacks to diagnose
155
Q

what is the presentation of classical trigeminal neuralgia

A
  • at least 3 attacks unilateral face pain
  • occurring in one or more distributions of trigeminal nevre, with no radiation beyond trigeminal distribution
  • pain has at least 3 of 4 characteristics
    1. recurring in paraoxysmal attacks from a fraction of a second to 2 minutes
    2. severe intensity
    3. electric shock like, shooting, stabbing or sharp
    4. precipitated by innoculus stimuli to affected side of face
156
Q

what are the features of medication overuse headache

A
  • present for >15 days/month
  • regular use for >3months of one or more symptomatic treatment drugs
  • e.g triptans, opioids, combination analgesics
  • headache worse during drug use
157
Q

what is the difference between an ischaemic and haemorrhagic stroke

A
  • ischaemic - obstruction within a vessel supplying the brain
  • haemorrhagic - when a weakened blood vessel ruptures
158
Q

what is a TIA

A
  • transient ischaemic attack - caused by temporary interruption of blood flow with stroke like symptoms but doesn’t damage brain cells or cause permanent disability
159
Q

if a patient had a stroke in the anterior cerebral artery, what symptoms would be seen on examination

A

-anterior cerebral supplies midline of frontal lobe (motor) and superior medial parietal lobe (sensory)
causes
- leg weakness ( legs are supplied by midline of brain – HOMUNCULUS)
- sensory disturbance in legs
- gait apraxia
- incontience
- drowsiness
- akinetic mutism (decrease in spontaneous speech)

160
Q

if a patient had a stroke in the middle cerebral artery, what symptoms would be seen on examination

A

middle cerebral supplies the lateral part of both lobes

  • contralateral arm and leg weakness
  • contralateral sensory loss
  • hemianopia
  • aphasia (language impairement)
  • dysphasia
  • facial droop
161
Q

if a patient had a stroke in the posterior cerebral artery, what symptoms would be seen on examination

A

posterior cerebral supplies the occipital lobe, inferior temporal lobe and various deep structures such as thalamus

  • motor deficits such as hemiparesis or tetraparesis + facial paresis 40-67% of cases
  • dysarthria (unclear articulation of speech)
  • vertigo, nausea and vomiting
  • visual disturbances
  • altered consciousness
162
Q

what are the differentials of stroke

A
  • head injury
  • hypo/hyperglycaemia
  • subdural haemorrhage
  • intracranial tumours
  • encephalitis
163
Q

what are the modifiable risk factors for stroke

A
  • hypertension
  • smoking
  • DM
  • heart disease
  • PVD
  • inc PCV
  • inc lipids
  • inc alcohol use
164
Q

what are the tests for stroke

A

EXAMINATION
CT to tule out primary haemorrhage
MRI

165
Q

what is the management of a stroke

A

Thrombolysis

  • I.V. alteplase
  • CI - recent surgery 3 months, recent arterial puncture, anticoagulant use, severe liver disease, acute pancreatitis, clotting disorder

risk management

  • aspirin (COX1 inhibitor)
  • clopidogrel
  • statin
  • warfarin and NOAC’s (AF treatment) anticoagluant
  • antihypertensives
166
Q

what are the causes of stroke

A
  • small vessel occlusion
  • CNS bleeds
  • cardiac: non valvular AF, prostehtic valves, IE, patent foramen ovale
167
Q

what is the presentation of a TIA

A
  • usually embolic
  • <24 hours
  • signs specific to the arterial territory involved
  • amaurosis fugax occours when the retinal artery is occluded, causing unilateral progressive vision loss like a curtain descending
  • global events e.g syncope, dizziness are NOT typical pf TIA’s
168
Q

what are the causes of TIA

A
  • atherothromboemolism from carotid chief cause - listen for bruits
  • cardioembolism
  • hyperviscosity e.g polycythaemia, myeloma, sickle cell
  • vasculitis
169
Q

what are the differentials of a TIA

A
  • hypoglycaemia
  • migrane aura
  • focal epilepsy
  • hyperventilation
  • retinal bleeds
170
Q

what are the tests for TIA

A
  • FBC
  • ESR
  • U+E
  • glucose
  • lipids
  • CXR
  • ECG
  • carotid doppler +/- angiography
  • CT or diffusion weighted MRI
  • echo
171
Q

when should TIA lead to emergency referral

A

4 or more = HIGH RISK OF STROKE
6 or more = STRONGLY PREDICTED
ABCD^2

Age - 60 or above (1)
BP - 140/90 or above (1)
Clinical features
- unilateral weakness (2)
- speech disturbance no weakness (1)
Duration of symptoms 
- 1 hour or more (2)
- 10-59 mins (1)
Diabetes (1)
172
Q

describe the features of huntingtons disease

A
  • autosomal dominant
  • repeat of CAG on chromosome 4 - 36 repeats
  • neurodegenerative disease
  • prodromal depression, irritibility, aggitation
  • progresses to chorea (– involuntary rapid irregular jerky movements mainly of the face and limbs) dementia and fits
  • atrophy + neuronal loss of striatum and cortex
  • sulpriamide and olanzapine (antipsychotic) and also helps weight gain
173
Q

what is the presentation of cauda equina

A
  • alternating or bilateral root pain in legs
  • areflexic paralysis of the legs
  • saddle anaesthesia (perianal)
  • loss of anal tone on PR
  • bladder and bowel incontinence
  • legs flaccid and areflexic
174
Q

what are the causes of cauda equina

A
  • maligancy
  • congential lumbar disc disease
  • lumbosacral nerve lesions
175
Q

how should cauda equina be treat

A
  • urgency dexamethasone in malignancy

- if abscess compress and give antibiotics

176
Q

what is the management of TIA

A
  • of risk factors -antihypertensives, management of DM and hyperlipidaemia
  • antiplatelets - aspirin 300mg for 3 weeks then clopidogrel 75mg
  • anticoagulants if cardiac source of emboli
  • carotid endarterectomy

Phase2a (10 decks)

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