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Phase 3A 'The List' conditions > Neurology notes > Flashcards

Neurology notes Flashcards

1
Q

3 big causes of TLOC?

A

Epileptic seizure, syncope and psychogenic non-epileptic seizure

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2
Q

What is a seizure? Types of epileptic seizures?

A

An abnormal and excessive discharge of cerebral neurones
Focal- simple partial (aura)
Complex partial–> LOC, some motor manifestation, lip smacking, fiddle with buttons/ fingers
Secondary generalised tonic clonic seizures

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3
Q

Generalised onset of epileptic seizures? Causes?

A

Generalised tonic clonic seizures - GTCS, myoclonic jerks, absences
Idiopathic/ genetic cause, early morning seizures, worse with sleep deprivation/ alcohol, photosensitivity

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4
Q

Different syncope types?

A

Reflex- neurally mediated, vasovagal, situational, carotid sinus hypersensitivity, cardiogenic, orthostatic hypotension- drugs, autonomic failure

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5
Q

Conditions predispose to transient tachyarrhythmias? These have an abnormal what between events?

A

Bradyarrhythmias, cardiac ischaemia, structural heart disease
ECG- cause sudden death in young people, do ECG in patients with TLOC

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6
Q

Heart block types that have a high risk of progression to asystole?

A

Complete (3rd degree) heart block, Mobitz type II 2nd degree heart block, incomplete trifascicular block- RBBB, LAD, 1st degree heart block

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7
Q

Why does acute ischaemia cause syncope? Blackout during exercise= what until proven otherwise?

A

Arrhythmia, output failure/ acute mitral regurgitation

Cardiogenic

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8
Q

PNES= associated with what?

A

Comorbid psychopathology and childhood sexual abuse

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9
Q

Rarer causes of TLOC? Useful past medical hx features? Drug hx? Social hx? Family hx?

A

Hypoglycaemia and acute hydrocephalus
Birth- premature/ SCBU, febrile seizures, CNS infections/ head injury, psychological comorbidity
Antidepressants, tramadol
Psychological comorbidity, alcohol and drugs, driving
Seizures, sudden cardiac death, evidence of psychological comorbidity

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10
Q

Hx for GTCS?

A

No trigger, may have aura, stiffening, jerking of limbs, vocalisation/ grunting breathing, cyanosis, eyes open, 1-2 minutes long, profound confusion for about 20 minutes, lateral tongue bite, urinary incontinence, injury
FH- seizures, tramadol e.g., head injury

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11
Q

Hx for syncope?

A

Triggers for vasovagal/ none for cardiac, typical fainting syndrome, may have jerks if maintained upright posture, pallor, brief, rapid recovery, previous events, cardiac hx, hypotensive meds, family hx of sudden cardiac death

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12
Q

Hx for PNES?

A

May be situational, symptoms= discussed sparingly, eyes often closed, may be emotional/ partially responsive, often very prolonged, apparent status epilepticus, variable post-ictal phase- almost always tired/ washed out
Psych comorbidity, other functional illness, antidepressants, psychosocial deprivation/ domestic abuse, trauma, FHX

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13
Q

All patients with TLOC should have what? CT not in syncope unless what? Epilepsy patients neuroimaging unless diagnosis of what? Ix of choice?

A

A 12 lead ECG
Acute hydrocephalus suspected
Genetic generalised epilepsy
MRI

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14
Q

Normal EEG does not do what? Gold standard diagnosis for PNES?

A

Exclude epilepsy

Video EEG recording in hospital

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15
Q

6 types of neurological emergencies?

A

Coma, sudden/ subacute new headache
Weakness a) generalised +/- resp failure, acute/ subacute paraplegia/ quadriplegia, acute hemi/ monoplegia
Visual loss
Status epilepticus
Other- bladder function loss, hemiballismus, status dystonicus, severe chorea, severe dysphagia, acute dysphasia

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16
Q

Common coma causes? Uncommon? Rare?

A

Drugs, toxins, anoxia, mass lesions- bleeds, infections, infarcts, metabolic, SAH, epilepsy
Mass lesions- tumours, venous sinus occlusions, hypothermia, psych- catatonia
Pituitary apoplexy, fat embolism

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17
Q

Examination in coma?

A

GCS, pupils- size, reactions, movements, corneal reflexes, focal deficits- asymmetry motor function, tendon reflexes, plantar responses, meningism

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18
Q

Assessing coma?

A

Blood tests, imaging- CT, MRI, lumbar puncture, EEG

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19
Q

What is status epilepticus?

A

Persistent seizure activity for 30 mins/ more, continuous, intermittent without recovery of consciousness
20% cases= fatal, increased CNS metabolic consumption, rhabdomyolysis, renal failure, metabolic acidosis, hyperthermia, heart and other organ effects

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20
Q

What is sudden onset headache with third nerve palsy/ painful 3rd CN palsy until proven otherwise? Causes of sudden severe headaches?

A

SAH
Cerebral venous sinus thrombosis, dissection- carotid/ vertebral, infection, acute haemorrhage/ acute infarcts, pituitary apoplexy

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21
Q

Presentation spontaneous SAH? On examination?

A

Acute severe localised headache, meningism, double vision, droopy eyelid
Sometimes seizures, low GCS, sudden death
Normal/ reduced GCS, subhyaloid haemorrhage, 3rd nerve palsy, bilateral extensor plantar responses, severe meningism, focal neurological deficit

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22
Q

Investigations for SAH?

A

Immediate- CT, CT angiogram/ MRI angiogram, lumbar puncture- 12 hours after for xanthochromia, catheter angiogram

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23
Q

Features of GBS? GBS mimics?

A

Acute/ subacute, demyelinating> axonal, immune mediated, multifocal polyradiculo-neuritis
Numbness starting distally, progressive ascending weakness, bifacial weakness+ other cranial neuropathies, flaccid tetra/ paraparesis, areflexia
Spinal shock syndrome secondary to cord compression, botulism, MG

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24
Q

Ix for GBS? Tx?

A

CSF- elevated protein, fewer <3/ no cells
Monitor vital capacity, DVT prophylaxis, BP, ECG, monitor swallow- low threshold for NG feeding
IVIG- 2g/ kg total dose, over 5/7, plasma exchange-less available, alternate days for 5-7 exchanges

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25
Q

What are the descending (motor tracts)?

A

Anterior and lateral corticospinal tracts, medial and lateral reticulospinal tracts, vestibulospinal tract, oliviospinal tract, tectospinal tract, rubrospinal tract, tectospinal tract

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26
Q

Ascending (sensory tracts)?

A

Fasciculus gracilis, fasciculus cuneatus, anterior and posterior spinocerebellar tracts, spinotectal, lateral and anterior spinothalamic tracts

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27
Q

Causes of spinal cord disorders?

A

Traumatic- whiplash, gunshot, stab, haematoma, degenerative- cervical and lumbar spondylosis, inflammatory- MS, transverse myelitis, neoplastic- ependymoma/ meningioma, infective- HIV, vascular- anterior spinal cord artery occlusion, spinal dural fistula, granulomatosis- sarcoidosis, metabolic- vit B12 deficiency, hereditary, neurodegenerative- ALS, other- syringomyelia

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28
Q

Symptoms of a spinal cord emergency? Need to rule out what?

A

Acute/ subacute onset: bladder- bowel weakness, saddle anaesthesia, leg weakness, constant sensory deficit, significant pain–> acute imaging of spine (MRI)
Cord compression

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29
Q

Investigating traumatic spinal cord disorders? Degenerative? Inflammatory? Neoplastic?

A

MRI
MRI, CT spine
MRI spine, then brain with contrast, LP- OCB and cells
MRI W/ contrast

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30
Q

Investigating infective spinal disorders? Vascular? Granulomatous? Metabolic? Hereditary? Other neurodegenerative? Other?

A 
MRI, ESR, BBV, FBC
MRI, angiography, vasculitis screen
Serum ACE level, MRI, CXR
B12, folate MMA and fasting homocysteine
Genetic panel
EMG and genetics
MRI
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31
Q

Lesion of dorsal lesion–>? Common causes? Below T6, only what is present?

A

Ipsilateral loss of light touch, vibration and position sense in right leg, generalised below the lesion level
MS, penetrating injuries, compression from tumours
Fasciculus gracilis

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32
Q

Lesion of right fasciculus cuneatus at C3? Common causes?

A

Absence of light touch, vibration and position sensation in right arm and upper trunk
MS penetrating injuries, compression from tumours

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33
Q

Lesion of right lateral corticospinal tract at L1? Right lateral spinothalamic tract at L1?

A

UMN signs in right leg

Absence of pain and temperature sensation in left leg

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34
Q

Damage to anterior gray and white commissures (central cord syndrome) at C5-C6 causes what? Causes?

A

Absence of pain and temperature sensation in C5 and C6 dermatomes in both upper extremities
Post traumatic contusion and syringomyelia, intrinsic spinal cord tumours

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35
Q

Complete transection of right half of spinal cord at L1?

A

Absence light touch, vibration and position sense in right leg, UMN signs in right leg, absence of pain and temperature sensation in left leg

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36
Q

Complete transection of spinal cord at L1?

A

UMN signs in both legs (paraplegia,) absence of pain, temperature sensation, light touch, vibration and position sense in both legs

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37
Q

Complete transection of dorsal columns bilateral in cervical region (posterior cord syndrome)?

A

Absence of light touch, vibration and position sense from neck down- below lesion level

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38
Q

Anterior cord syndrome in cervical region?

A

UMN signs bilaterally below lesion level, LMN signs bilaterally at lesion level
Absence pain and temperature sensation bilaterally below lesion
Light touch, vibration, position sense= intact throughout

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39
Q

Causes of anterior spinal artery occlusion?

A

Vasculopathy- stroke risk, accidental occlusion of artery of Adamkwich during AAA repair

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40
Q

Common causes of transverse myelitis? Hemi-section of the cord?

A

MS, post infectious transverse myelitis, ADEM, other inflammatory- sarcoidosis
Intervertebral disc protrusion, spinal cord tumours, metastatic deposits, abscess

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41
Q

Causes of cauda equina?

A

Compressive- discs+ tumours, non-compressive- inflammatory, infiltrative, granulomatous, vascular- spinal dural fistula

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42
Q

Management of spinal cord disorder?

A

Manage the cause and complications- weakness, bladder and bowel dysfunction, spasticity, pain, pressure areas, mobility

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43
Q

Symptoms of carotid territory stroke? Posterior circulation?

A

Weakness of face, leg, arm, amaurosis fugax, impaired language
Dysarthria, dysphagia, dysarthria, diplopia, dizziness, ataxia, diplegia

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44
Q

All 3 symptoms needed for diagnosis of a TACS? 2 symptoms needed for what diagnosis?

A

Homonymous hemianopia, unilateral weakness and/ or sensory deficit of face, arm and leg, higher cerebral dysfunction- visuospatial disorder/ dysphasia
PACS

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45
Q

One of what symptoms needed for a POCS diagnosis?

A

Cranial nerve palsy and a contralateral motor/sensory deficit
Bilateral motor/sensory deficit
Conjugate eye movement disorder (e.g. horizontal gaze palsy)
Cerebellar dysfunction (e.g. vertigo, nystagmus, ataxia)
Isolated homonymous hemianopia

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46
Q

One of what symptoms needed for a LACS diagnosis?

A

Pure sensory stroke
Pure motor stroke
Sensori-motor stroke
Ataxic hemiparesis

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47
Q

Time-window for mechanical thrombectomy for anterior circulation stroke?

A

6 hours- can be used alongside IV thrombolysis

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48
Q

Medical management of strokes?

A

VTE assessment, hydration, NG feeding +/- PEG feeding, spasticity- physio, botox, monitoring for infection

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49
Q

Secondary prevention in strokes?

A

Antiplatelets- 300mg aspirin 2 weeks, clopidogrel lifelong
Anticoagulation- in AF, HASBLED and CHADSVASC scores
BP< 130/80 in HTN
Cholesterol- statin therapy, 40% reduction in non-HDL cholesterol

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50
Q

Surgical tx of stroke?

A

Extracranial carotid stenosis= USS carotid dopplers+/- CTA/MRA, carotid endarterectomy/ stenting
Malignant MCA syndrome- decompressive hemicraniectomy
Posterior circulation= EVD/ posterior fossa decompression

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51
Q

Stroke mimics?

A

Seizures, tumours/ abscess, migraine, metabolic, functional, spinal cord/ peripheral nerve/ cranial nerve

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52
Q

Muscle weakness hx?

A

Onset- instant/ gradual
Distribution- proximal/ distal, symmetrical/ asymmetrical, mono/ poly
Cranial nerve involvement, variability
Sensory symptoms, recent illness, PMH, FH, drugs, alcohol

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53
Q

Peripheral neuropathy more motor loss?

A

GBS, CIDP, C-M-T disease, diptheria, porphyria

Deficiency states, diabetes, alcohol/ toxins/ drugs, metabolic abnormalities, leprosy, amyloidosis

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54
Q

Presentation of MG?

A

Generalised, fatiguable weakness, proximal limbs, neck and face, extraoccular, bulbar particularly elderly, occular= 10-25%

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55
Q

Investigation for MG? Tx?

A

Tensilon test, AChR antibodies, EMG, CT thorax
ACHesterase inhibitors e.g. pyridostigmine
Immunosuppressants- steroids, azathioprine, thymectomy

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56
Q

MND presentation?

A

No sensory/ visual/ B/B involvement, asymmetric weakness, bulbar/ limb onset, survival= usually 2-5 years

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57
Q

Common muscle disorders? Uncommon?

A

Steroid myopathy, statin myopathy, metabolic and endocrine myopathies, myotonic dystrophy
Duchenne, Becker, polymyositis, mitochondrial disorders

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58
Q

Investigation muscle disorders? Tx?

A

CK, EMG, ESR/ CRP +/- genetics, +/- biopsy

Remove causal agent, supportive, immunosuppress if inflammatory

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59
Q

Red flags for headaches? Weakness?

A

New headache> 60 y/o, thunderclap, infective sx, hx of malignancy
Loss of sphincter control, sudden onset, progressive, respiratory/ swallowing issues

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60
Q

Approach when the patient is alert/ orientated? Drowsy/ confused/ unconscious?

A

Hx and neuro-examination

Collateral hx, gen app, vital signs and mini-neurologic exam: GCS, lateralising signs, pupils

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61
Q

Use what if patient can give a history? Can’t give a hx?

A

‘Pain tool,’ ‘domain tool,’ and standard background history headings with neuro-examination= general appearance, vital signs and core examinations based on possible syndromes
Collateral hx, exam= general appearance, vital signs and mini-neurologic exam= GCS, pupils and lateralising signs

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62
Q

Sub-headings for best motor response out of 6? How do this? How long post-ictus?

A

6= obeys commands, 5= localises to pain, 4= flexes to pain, 3= withdrawal, 2= extends to pain, 1= none
Groove behind ears both sides top of the bed
1 hour

63
Q

Sub-headings for best verbal response out of 5?

A

5= orientated in time, place and person, 4= confused, 3= inappropriate words, 2= incomprehensible sounds, 1= none

64
Q

Sub-headings for best eye opening response out of 4? Can only do what after giving anaesthetic?

A

4= eyes open spontaneously, 3= eyes open to speech, 2= eyes open to pain, 1= none
Pupils

65
Q

About identifying what in a pupil examination? Usually represents what?

A

‘Fixed and dilated pupil’
Compression from the brain above, on the PARASYMPATHETIC fibres on the outside of the third nerve as it passes over the apex of the petrous part of the temporal bone, due to some life-threatening brain swelling process

66
Q

How long once unilateral fixed and dilated pupil developed to provide lifesaving surgical intervention? This time window can be maximised by what and time to do what?

A

A 3-4 hour window before contralateral pupil fixes and dilates and death is inevitable
IV mannitol administration, have the patient intubated/ ventilated, scanned and transferred to a neurosurgical centre

67
Q

What does a lateralising sign reflect? They tend to be obvious during what process? Such signs include what?

A

A problem with one hemisphere versus the other
During the process of doing the GCS assessment
Inattention to one side, gaze paresis (unable to look) to one side
An upper limb drift in an individual who can hold out his arms with eyes closed i.e. obeys commands, slower localising/ flexion response of one upper limb versus the other when both are either localising/ flexing, asymmetric motor response of one upper limb versus the other e.g. one side flexing, the other extending

68
Q

Pain tool in history taking?

A

Site, radiation, onset- sudden/ gradual, precipitating factor, duration, course, progression, character, severity, disturbing sleep, alleviating/ exacerbating factors, associated symptoms, had before, response to conservative measures, significantly interfering with lifestyle

69
Q

Domain tool to explore impact on person’s lifestyle?

A

Mobility, communication, interpersonal relationships, school/ work/ hobbies, continence/ sexual function/ personal hygiene, sleep, eating/ drinking/ nutrition

70
Q

What appears first in general- signs or symptoms? 2 exceptions? How to neuro-examine a child?

A

Symptoms
Watch them as you lead them through structured play and then do ‘core examination’ and vital signs at end to minimise distress

71
Q

What is a secondary brain problem? Primary? What’s important in looking to identify primary brain problems?

A

Where the pathological process disrupting brain function= outside the brain e.g. hypovolaemia/ hypotension/ shock, hypoxia
Within the brain
Vital signs- e.g. pyrexia for CNS infection, irregular pulse (AF) in context of a stroke

72
Q

What’s involved in the core neurologic examination?

A

General appearance, vital signs, gait, fundoscopy, long tract signs and vibration sense with 125 Hz tuning fork

73
Q

Long tract signs useful in screening for what? What are they?

A

Myelopathy
Spastic gait, hypertonia, hyper-reflexia, Babinski’s, clonus, cross-abductors, Hoffman’s sign, loss of fine finger movements, deltopectoral reflex

74
Q

Headings for neuro-exam beyond the core exam?

A 
Head/ cranial nerves
Upper limbs
Lower limbs
Trunk: 1. Spinal deformity
2. Sensory level
3. Surgical wounds
4. Paraspinal mass
5. Truncal flexion
6. Paravertebral muscle spasm
7. NF1 skin lesions, e.g., cafe au lait
8. Palpable/percussable bladder
9. Patulent anal sphincter
10. Urostomy, colostomy
11. Perineal sensation
12. Dysraphism, e.g., any dimple, pit, hairy patch or swelling in midline down spine
75
Q

Format for presenting findings?

A

Name, age, PC, when started
Described pain as…
Smoker, allergies, living condition, past surgery, occupation, clinically- well/ unwell, general appearance, vital signs, positive findings, negative findings

76
Q

What is a benign essential tremor?

A

A fine tremor affecting all the voluntary muscles- symmetrical, most notable in the hands, but affects many other areas e.g. head tremor, jaw tremor and vocal tremor
Worse when tired, stressed/ after caffeine, improved by alcohol, absent during sleep

77
Q

What is an intention tremor?

A

Broad, coarse and low frequency tremor evidence during deliberated movement, usually perpendicular to the direction of movement

78
Q

What is an essential tremor? What is an action tremor?

A

Involuntary and rhythmic shaking, during drinking from a glass/ tying shoelaces- both hands and arms, often more noticed more in dominant hand as it is an action tremor

Occurs with the voluntary movement of a muscle e.g. intention

79
Q

What to check with essential tremor? % responds to medication? What meds?

A

U&Es, LFT, TFT, calcium
50%
Propanolol, primidone, pregabalin, gabapentin, clonazepam

80
Q

Which tremors should be referred?

A

All new ones not essential tremor, diagnostic uncertainty, essential requiring further management, with other neurological symptoms: ataxia, cerebellar signs, parkinsonism

81
Q

E.g. of Parkinsonism?

A

Rigidity, bradykinesia, gait shuffling, tremor: idiopathic Parkinson’s, vascular, NPH, Parkinson’s plus, iatrogenic

82
Q

Stages of Parkinson’s?

A

Early ‘honeymoon period’, middle period- wearing off, late period- dyskinesias, chorea, fluctuations, cognitive impairment

83
Q

Drugs used in Parkinson’s? What is entacapone?

A

Co-careldopa/ co-beneldopa, CR preparation, dispersible prep- resuce/ morning, Stalevo= co-careldopa plus entacapone
A COMT inhibitor- prevents levodopa breakdown in brain and periphery

84
Q

Non-ergot and ergot dopamine agonists for Parkinson’s? What do ergot drugs require?

A

Ropinirole, pramipexole, rotigotine
Bromocriptine, pergolide, cabergoline
Monitoring

85
Q

Pros and cons of dopamine agonists over levodopa?

A

Less dyskinesia, longer acting

More risk of hallucinations, compulsive behaviour, postural hypotension, daytime sleepiness, specific ergot SEs

86
Q

E.g. of MAOIs? Beware of what? CIs?

A

Selegiline, rasagiline- NICE= SSRI best avoided, citalopram relatively safe
Serotonin syndrome with SSRI and tricyclics
Tramadol, pethidine, methadone

87
Q

What is apomorphine?

A

Water soluble dopamine agonist- rescue tx in pen form, continuous daytime infusion- helps smooth motor fluctuations, less hallucinogenic than other dopamine agonists

88
Q

Amantadine can help what? New drugs? Drug with most improvement of motor symptoms? Intermediate? Least? Most best on comb of what?

A 
Dyskinesia
Safinamide, opicapone
Levodopa
Dopamine agonists
MAOIs
Levodopa and a dopamine agonist
89
Q

NICE recommendations for Parkinson’s?

A

Refer to specialist for diagnosis untreated, if motor fluctuations- manage according to specialist advice
Point of contact to specialist services
Review every 6-12 months
Document impulse control disorder, sleep attacks and hallucinations, consider DAT Spect in atypical tremors
Access to physio, OT, SALT, dietician, advise vit D supplementation, palliative care referral and end of life

90
Q

Parkinson’s non-motor symptoms?

A

Mood, sleep, cognitive disorders, impulse control, autonomic dysfunction, presymp symptoms

91
Q

Manage who as non-PD patients? Sleep issues? Tx? Causes?

A

Anxiety and depression
Insomnia, daytime sleepiness, disruptions during sleep, REM sleep behaviour disorder
Clonazepam, melatonin
Lack of muscle and mental relaxation, stiffness, restless, tremor, meds wear off

92
Q

Daytime sleepiness requires what? Night time akinesia?

A

Med review- modafinil

Med review- CR levodopa, rotigotine patch

93
Q

What to do with cognitive disorders in PD?

A

Review triggering factors and non PD medication and refer to neurology
Mild-moderate PD dementia= cholinesterase inhibitors, referral to dementia pathway, memantine if not tolerated

94
Q

What to do with psychotic Parkinson’s patient?

A

Provoking factors, refer to neurology, specialist can discontinue drugs, initiate quetiapine, clozapine, cholinesterase inhibitors

95
Q

AN symptoms of Parkinson’s? Tx?

A

Orthostatic hypotension, constipation, nausea, vomiting, heat intolerance, urinary frequency and incontinence, urinary urgency, nocturia, sweating, hypersalivation, drooling, seborrhoea, sexual dysfunction in men and women
Anti-emetics, stop anti-HTs, anticholinergics, botulinum/ hyoscine

96
Q

Clinical syndromes?

A

1) Proximal myopathy
2) Myasthenic syndrome
3) Mononeuropathy
4) Peripheral neuropathy
5) Radiculopathy
6) Anterior horn cell syndrome
7) Myelopathy
8) Vertebral pain syndrome
9) Cerebellar syndrome
10) Cranial neuropathy
11) Lobe syndrome
12) Parkinsonism
13) Chorea
14) Parasellar syndrome
15) Dementia
16) Acute confusional state
17) S+S of raised ICP
18) Epilepsy
19) Stroke
20) Meningism/ meningeal irritation
21) MS
22) Somatisation

97
Q

Pattern and cause of proximal myopathy? O/E?

A 
Progressive pattern (hair, stairs and chair,) secondary to corticosteroid use 
Balance and single leg squat
98
Q

Most common upper limb mononeuropathies? Lower limbs? Investigations?

A 
Carpal tunnel (thumb, index and middle finger,) ulnar nerve and axillary due to shoulder dislocation/ relocation, radial neuropathy due to spiral fractures of the radius
Common peroneal nerve= rare cause, meralgia paraesthetica in obese people
EMG/ nerve conduction studies
99
Q

Causes of peripheral neuropathy?

A

Diabetes mellitus and leprosy- mixed motor and sensory

100
Q

What is a radiculopathy? Symptoms of radiculopathy? Commonly affected upper and lower limb?

A

Pinching of a nerve root in the spinal column

Radiating limb pain often in the pattern of the dermatome- sharp/ shooting, C6/7= common, L5/S1

101
Q

What is spinal claudication and what is it associated with?

A

Radiculopathic subsyndrome- bilateral radiating leg pain/ paraesthesia that comes on with walking and they have to stop and rest for a number of minutes before walking on again, often relieved by leaning forward i.e. cycling is not an issue

102
Q

Red flag symptoms for a radiculopathy?

A

Constant bilateral radiating leg pain, perineal numbness, foot weakness, and urinary symptoms

103
Q

Myotomes and dermatome for C6? Reflex?

A

Biceps
Thumb
Biceps jerk

104
Q

Myotomes and dermatome for C7? Reflex?

A

Triceps
Middle finger
Triceps jerk

105
Q

Myotomes and dermatome for L5?

A

Dorsiflexion (stand on heels), dorsum of foot/ big toe

106
Q

Myotomes and dermatome for S1? Reflex?

A

Plantarflexion- stand on toes

Ankle, lateral foot/ sole of foot/ little toe

107
Q

What is a residual radiculopathy?

A

No active nerve root compression, left with deficit

108
Q

Underlying disease entities for anterior horn cell syndrome?

A

MND, spinal muscular atrophy and poliomyelitis

Areflexia, flaccid paralysis, sensation= preserved, LMN signs

109
Q

What is a myelopathy? Causes and commonest cause? Important to screen for what?

A

Injury to the spinal cord caused by severe compression- from spinal stenosis, disc degeneration, disc herniation, AI disorders/ other trauma
Disc-osteophyte cord compression
Long tract signs

110
Q

Who should be screened for myelopathy? What will they complain of? Where is the lesion in a C5/6 myelopathy?

A

Anybody attending with neck pain/ back pain or radiating arm or leg pain
Clumsy hands, stiff legs/ not their own
C6

111
Q

What will a patient complain of with vertebral pain syndrome? O/E? Underlying disease entity?

A

Localised aching pain with limited radiation, stiffness/ restriction of movement, worse with activity, absence of associated neurologic symptoms
Visible/ palpable paravertebral muscle spasm, tenderness and movement restriction
Wear& tear degenerative changes, rare= TB, bacterial discitis/ osteomyelitis, osteoporotic fractures/ metastatic disease (part thoracic vertebral pain.)

112
Q

Signs and symptoms of cerebellar syndrome?

A

Patient feels drunk, S+S= ipsilateral to side of lesion

Gait apraxia, ataxia on finger nose testing, and nystagmus

113
Q

Symptoms of frontal lobe syndrome? Parietal lobe?

A

Contralateral limb weakness, motor dysphasia for dominant frontal love(Broca’s area), personality only affected in bilateral frontal lobe process
Non-dominant= contralateral sensory disturbance- NO limb pain, dominant= as per non+ higher sensory processing- associated issues e.g. dyslexia, dysgraphia, dyscalculia and astereognosis

114
Q

Temporal lobe syndrome? Occipital?

A

Dominant= understanding of speech(superior temporal gyrus) and memory, no for non-dominant temporal lobe

Contralateral visual field loss

115
Q

What does parasellar syndrome include?

A

Hypopituitarism and bitemporal hemianopia

116
Q

Non-dementia causes of dementia? Difference with acute confusional state?

A

NPH, large frontal/ subfrontal or dominant hemisphere meningioma and subdural haematoma
Acute= often caused by secondary brain problem, lasts hours/ days, dementia= primary and lasts months/ years

117
Q

What will the patient complain of regarding raised ICP? O/E? Possible cause?

A

Gradual onset, progressive headache, nausea/ vomiting, double vision, blurred vision, general deterioration in cognitive functioning and mobility and LOC
Drowsiness, papilloedema, paralytic squint, fixed dilated pupil, reduced LOC
Hydrocephalus, CNS bacterial infection- brain abscess, empyema, meningitis

118
Q

3 categories of stroke?

A

SAH, ischaemic stroke, spontaneous brain parenchymal haemorrhage

119
Q

Who go to neurosurgery for surgical decompression of an ischaemic stroke?

A

Those with a major intracranial vessel stroke with a large stroke of secondary brain injury and swelling–> critically raised ICP
Common= small artery–> internal capsule= taken out, no large volume of brain tissue injury/ swelling

120
Q

Indications for surgical decompression in ischaemic stroke?

A

Cerebellar infarction- tight posterior fossa and secondary hydrocephalus on imaging, can be from vertebral artery dissection, MRI can confirm
Infarction in territory of MCA- in at least 50% MCA territory, patient <60 y/o, deteriorating LOC, referral within 24 hours symptom onset, surgery within 48 hours

121
Q

Carotid endarterectomy in ischaemic stroke associated with what? What should be done within one week of symptom onset? Consider in who? Surgery within how long in TIA/ minor stroke?

A

Carotid arter stenosis in the neck- 75% patients, Carotid imaging
Symptomatic carotid stenosis 50-99%
2 weeks

122
Q

Clinical syndrome presentation in supratentorial haemorrhage? Infratentorial? Angiographic investigations if what planned and possibility of what? Blood tests?

A

Lobe syndrome, meningeal irritation, raised ICP
Cerebellar syndrome, meningeal irritation, raised ICP
Surgery, underlying AVM/ aneurysm
Platelet count and clotting factors

123
Q

Management of a stroke?

A

Reverse anticoagulation/ address bleeding diathesis, uncontrolled HTN= titrated in critical care setting with IV labetalol and monitor, significant haemorrhage discussed with neurosurgeon, reducing LOC (mass effect/ secondary hydrocephalus)= surgery, brainstem= poor prognosis, surgical evacuation= no benefit in limb weakness/ neurological deficit
Exclude any underlying causative lesion such as tumour/ AVM

124
Q

SAH presents how? Investigations?

A

Occipital headache- worst ever, vomiting, photophobia and neck stiffness
CT head- negative= lumbar puncture for xanthochromia, +ve= CT angiography and/ or catheter cerebral angiography

125
Q

Classification of SAH? RFs for aneurysm formation? Where are aneurysms usually? Rare causes? Angiogram -ve in what %?

A 
Intracranial berry aneurysm 80-90%
Family history, HTN, smoking
At junction points around circle of Willis/ at main MCA bifurcation
AVM, arterial dissection, tumour
10%
126
Q

Management of SAH?

A

Dealing with comps of aneurysmal SAH and securing causative berry aneurysm at an appropriate time point

127
Q

How is an intracranial berry aneurysm secured? Reason for securing? Depends on what factors?

A

Surgical craniotomy and applying sprung titanium clip to neck of aneurysm with intra-op microscope/ endovascular placement of fine platinum coils inside lumen of aneurysm

Risk of rebleed and risk of further risk to life
Timing of the bleed with respect to presentation, background general health, SAH clinical grade- based on GCS, angiographic appearances, presence of angiographic arterial spasm

128
Q

Complications of SAH? Given pre-emptively in vasospasm? Management?

A

Hydrocephalus requiring insertion of external ventricular drain
Haematoma needing craniotomy and evacuation
Hyponatraemia- from cerebral salt wasting
Vasospasm–> infarction
Lower RTI

Nimodipine, driving BP with IV fluids and inotropes with arterial and central venous lines in situ, unless infarction on imaging

129
Q

What will patient complain of with meningeal irritation? O/E? Underlying disease entities?

A

Severe headache, vomiting, photophobia, neck stiffness, sudden onset if SAH
Drowsy, pyrexia if bacterial meningitis, photophobic, neck stiffness
SAH and bacterial meningitis= serious, CT then lumbar puncture

130
Q

Patients presenting to neurosurgery with otherwise unexplained symptoms should have a what to exclude MS?

A

MRI- discharged from neurosurgical follow-up

131
Q

% referred to neuroscience clinics have non-organic cause to neurologic symptoms? Further % have somatisation component?

A

10%

20%

132
Q

UMN issues with bladder? LMN? What tumour can cause brachial plexus issues?

A

Urgency and frequency
Cannot tell need the toilet, numbness
Those in the lung apex

133
Q

What two things can cause rhabdomyolysis? Colour of urine? Complications?

A

Drugs e.g. statins, corticosteroids and dehydration
Tea-coloured
Electrolyte imbalances, DIC

134
Q

Who would you give a CT head to?

A

In facial trauma, determine inflammation, plan radiation therapy for cancer, assess aneurysms, AVMs, assess bleeding/ clots, tumours and brain cavities- hydrocephalus

135
Q

Why over 65s scanned more readily? Primary and secondary brain injuries?

A

Tend to be on more drugs
Injury to scalp, fractures, haematomas, vascular injury
Hypoxia- ischaemia, swelling

136
Q

What is the Monro- Kellie doctrine?

A

Increase in brain tissue/ CSF/ blood must reduce the volume of another

137
Q

Look at what on CT head?

A

The scout film- fracture of upper cervical spine/ skull
Brain asymmetry
Sulci, Sylvian fissure and cisterns to exclude SAH
Change windows to look for subdural collection
Bone windows- fractures
Mass- intraaxial (in brain) or extraaxial

138
Q

Acute blood on CT head? Becomes isodense after how long? Then hypodense after?

A

Bright (hyperdense)
1 week
2+ weeks

139
Q

Extradural haematoma shape? Tx?

A

Boomerang

30cm 3 should be evacuated

140
Q

Subdural haematoma shape? White spot is what?

A

Crescent-shaped

Calcium calcification

141
Q

Look where for SAH on CT? See what?

A

Interpeduncular cistern and Sylvian fissure

Streaky blood into sulci of brain

142
Q

What is a contre-coup injury?

A

Opposite side to where trauma was

143
Q

Headaches+ other symptoms could be what? Often treated with what?

A

Venous sinus thrombosis

Heparin

144
Q

In acute stroke, initially tone is what? Becomes what? How do reflexes change?

A

Reduced, become increased

Areflexia–> hyperreflexia

145
Q

If can’t do MRI of the spine, do what?

A

CT myelography

146
Q

Start with what if acute head presentation? Worried about blood in the head? MS, sinus thrombosis or arterial dissection? Excluding/ better visualising pathology in posterior fossa?

A

CT head
CT
MRI
MRI

147
Q

Non acute head presentation? Spine presentation? Infection/ tumour?

A

MRI
MRI- CI–> CT myelogram
Include post-contrast

148
Q

2 golden rules for CNS imaging?

A

Always ensure a patient is ‘stable’ before transferring to the radiology department for scan- airway secure, vital signs= normal, scalp laceration= sutured
CT before LP

149
Q

4 Qs when viewing a CT scan?

A

Is there: 1) an intracranial mass- dimensions in three planes, surrounding oedema, loss of normal sulci/ gyri, loss of basal cisterns, ventricular effacement, midline shift in mm

2) Hydrocephalus- 3rd ventricle lost and temporal horns obvious?
3) Intracranial blood- patterns of haemorrhage, appearance of blood over time, white on ‘soft tissue window’, goes from white–> grey–> black
4) Skull and extracranial soft tissues

150
Q

10 common CT scan scenarios?

A

SAH, intraventricular haemorrhage, intracerebral haemorrhage, chronic subdural haematoma, extradural haematoma, acute subdural haematoma, brain abscess, malignant brain tumour, meningioma, obstructive hydrocephalus

151
Q

CSF colour in T2 MRI? Contrast that is given? Sequence for stroke/ abscess?

A

White
Gadolinium
DWI

152
Q

Seen on MRI for MS? To show spinal degenerative disease?

A

Axial, periventricular ‘high signal’ lesions on T2/ proton density
Sagittal T2 then axial T2

153
Q

4 concepts for looking at CT scans?

A

1) A simple matrix- of small squares that determine the resolution of the image and contain a value that represents amount of XR radiation by that square of tissue
2) Hounsfield units: bone= +1000, water=0, air= -1000
3) Grey scale: ‘soft tissue window’= brain/ blood/ CSF and ‘bone window’= skull detail
4) Neuroanatomy

154
Q

Two key Qs for patients and MRI?

A

Metal/ implants, is the patient claustrophobic

Phase 3A 'The List' conditions (8 decks)

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