Neurology Flashcards
(37 cards)
1
Q
American Spinal Injury Association impairment scale
A
complete (Grade A)
- complete sensory and motor deficit below lesion level
- in acute
- > reflexes are absent
- > no plantar response
- > tone is flaccid
- males may have priapism
- urinary and retention may occur
incomplete
- Grade B
- > sensory incomplete
- > loss of motor but not sensory below lesion level
- Grade C and D
- > both motor incomplete
- > vary by how many muscle groups remain >3+
2
Q
Central cord syndrome
A
- lesion encroaching on medial corticospinal tract/anterior horn gray matter
- > medially placed fibres disproportionately affected
- > greater weakness in arms than legs
- arching reflex fibres are disrupted
- > loss of reflexes below level
- disruption of crossing spinothalamic fibres
- > loss of pain/temp for adjacent dermatomes
- > retained above and below
- proprioception and vibration sense often spared
- urinary retention may occur
3
Q
Anterior cord syndrome
A
- injury to anterior spinal artery by retropulsed disc/bone fragment
- > loss of anterior two thirds of spinal cord tracts
- corticospinal
- > weakness and reflex changes
- spinothalamic
- > bilateral pain and temp loss
- autonomic tract
- > urinary incontinence
- gracile/cuneate tracts spared
- > retained touch, vibration, proprioception
4
Q
Spinal injury assessment
A
ABCD
-priority may be given to other life threatening injuries
Spinal precautions
- NSAID
- > neurological deficit
- > spinal pain
- > altered GSC
- > intoxication
- > distracting injury (extremity fracture)
- precautions
- > rigid cervical collar
- > log roll
- > spinal board
- > can use straps and blocks
- removing precautions
- > non of above criteria
- > full range of neck movement
Imaging
- not required for people with no NSAID criteria
- axial CT first line
- > superior to xray
- > poor with soft tissue injury
- MRI
- > when suspected soft tissue injury
- flexion extension Xray
- > when CT clear
- > suspicion of ligament damage and dynamic instability
5
Q
chronic complications of c spine injury
A
C-Spine PINBOARDS
- cardiac
- > arrhythmias
- > MI
- spasticity
- pneumonia
- immobility
- > DVT
- > pressure ulcers
- neuropathic pain
- bowel and bladder dysfunction
- osteoporosis
- autonomic dysreflexia
- resp failure
- > dyspnea
- > reduced exercise tolerance
- depression
- sexual dysfunction
6
Q
Clinical assessment of SAH
A
ABCDEFG
- AB = need for cardiorespiratory support
- C= heart rate and rhythm
- D= GCS, pupils (terson’s syndrome is vitreous haemorrhage with subarachnoid)
Hx
Presentation
- thunderclap “worst of life” headache
- onset with sex, emotions, exercise
- nausea and vom
- decreased level of consciousness
- meningismus
- neurological deficits
- seizure activity
- photophobia
Past medical sentinel bleed risk factors -previous bleed -family hx -smoking -heavy alcohol -hypertension -polycystic kidney disease -connective tissue disease -simpathomimetic drugs -anti-coags/anti-platelets
Exam:
Full neurological
- GCS
- focal deficits
- meningismus
- CNIV/CNVI palsy
Dilated pupil
- Torsens (=worse prognosis)
- papilloedema
7
Q
investigations SAH
A
Bedside:
-ECG (prolonged QT, ST segment abnorm)
Bloods:
- FBC (leukocytosis, platelets)
- Coags (associated coagulopathy)
- Trops (associated with higher mortality. seen inabsence of coronary artery disease)
- EUCs (hyponatraemia)
Imaging:
- CT brain (good sensitivity and specificity, decreases overtime)
- LP if CT normal: RBC count, clearing of blood from tubes 1-4, xanthochromia
8
Q
investigations TBI
A
Bedside:
- glucose
- opthalmoscope (papiloedema)
Bloods:
- FBC (anaemia, platelets)
- Coags
- EUC (renal function for investigations)
- LFTS (baseline, coag)
Imaging:
-CT non con
LP contraindicated with suspected ICP
9
Q
grading scale SAH
A
Hunt and Hess (looks at symptoms and motor deficit)
- grades 1-5
- asymptomatic and slight nuchal rigidity
- to deep coma, decerebrate
World Federation of Neurological Surgeons
- grades 1-5
- GCS 15 with no motor deficit
- to GCS 3-6 with or without motor deficit
10
Q
investigations meningitis
A
Bloods:
FBC (DIC and infection) -anaemia -leukocytosis -thrombocytopaenia CRP -when CSF gram stain neg., normal CRP almost excludes bacterial from viral cause VBG, or EUC and CMP -acidosis -hypokalaemia -hypoglycaemia -hypocalcaemia Coags with TT, fibrinogen, fibrin degradation products and D dimer (DIC) Blood culture consider serum procalcitonin (bacterial vs viral. more sensitive than specific)
Lumbar puncture
- opening pressure raised
- gram stain
- culture
- raised protein
- decreased glucose (CSF:serum glucose <0.6)
- pleocytosis (polymorph)
- lactate raised (distinguish aseptic from bacterial)
- latex agglutination (neisseria capsular polysaccharide antigen)
- PCR (more accurate for viral and bacterial infection)
Imaging
- CT brain when concerns for raised ICP
- underlying pathologies
- oedema and hydrocephalus common in meningitis
11
Q
prognosis SAH
A
- 50% mortality
- cognitive impairment 20%
- epilepsy increased risk
- risk of recurrence
12
Q
aetiology SAH
A
Aetiologies = A Past Vascular Defect
-Aneursymal (vast majority. mostly saccular, can be mycotic or fusiform)
-Perimesencephalic (most common non anneursymal)
-Vascular malformations
-Drugs (simpathomimetics)
also Tumors and Trauma
13
Q
pathophys SAH (saccular)
A
- formation of aneursym due to loss of internal elastic lamina and thinning of smooth muscle
- most aneursyms do not rupture
- association with site (more common in anterior circ but most likely to rupture in posterior circulation) and size
- Aneurysm develop over days. Initial size determined by structural forces. Will either rupture or harden. Larger aneursyms that have not ruptured are more likely (due to Laplace’s law) to continue growing, and rupture later. Supports finding that aneursyms that rupture late are larger than those that rupture early.
- Size greater than 1cm is increased risk
- Acute trigger usually (but not always) precedes rupture
14
Q
risk factors SAH
A
Risk factors for development of aneurysm:
- Family Hx
- Polycystic kidney disease
- Erhlers danlos
- Coarctation of aorta (HTN)
- Smoking
- HTN
- Post menopause estrogen decline
Risk factors for rupture/SAH
- Size
- posterior circ
- prior haemorrhage
- ETOH
- Simpathomimetic drugs
- Antithrombotic therapy
15
Q
ddx meningitis
A
encephalitis (confusion, mental state), meningitis, SAH
Infective meningitis
- infective
- > bacterial
- > viral
- > fungal
- aseptic
- bacterial parameningeal infection
- > epidural, subdural empyema
- > intracerebral abscess
Aseptic meningitis
- non infective
- > neoplasia (primary, secondary, haematological)
- inflammatory
- > SLE
- drug induced
- > NSAIDs
- > antibiotics
- > lamotragine
16
Q
seizure ddx
A
Some Crazy People Try To Mimic Seizure Movements
- syncope
- cardiac arrhythmia with syncope
- psychological (psychogenic, panic attack [hyperventilation, paresthaesia])
- TIA
- Transiant global amnesia
- Migraine aura
- Sleep disorder (narcolepsy, cataplexy)
- Movement disorder (tics, tremor, chorea)
17
Q
stroke aetiology
A
Ishaemic (85%) -thrombus ->arterial ->venous -embolic -systemic hypoperfusion Haemorrhagic (15%)
18
Q
classification of ischaemic strokes
A
TOAST classification (good inter-assessor reliability, guides treatment).
- large vessel infarct
- small vessel infarct
- cardioembolic
- other
- cryptogenic
19
Q
causes of ischaemic strokes
A
VEST
Thrombus:
- large vessel due to (A Very Disgusting FArt)
- > atheroma
- > vasoconstriction
- > dissection
- > fibromuscular dysplasia
- > arteritis, giant cell and takayasu
- small vessel (lacunar) due to Fat Little Arteries
- > lipohyalinosis
- > with fibrinoid degeneration
- > or artheroma
Embolic:
- 20% cardiac
- > AF
- > mural thrombus
- 10% carotid artery
- can be any artery to artery in cerebral circulation
Systemic hypoperfusion (watershed) due to
- PE
- tamponade
- arrhythmia
- MI
Venous thrombosis
-secondary to coagulation
20
Q
causes hemorrhagic strokes
A
Hypertensive Strokes Are Very Common
- Hypertension
- Simpathomimetic drugs
- Amyloid angiopathy
- Vascular malformation
- Coagulopathy (Warfarin, leukemia)
*typically in basal ganglia, thalamus, cerebellum and brainstem.
21
Q
causes of death and complications stroke
A
1st week -death due to stroke itself 2nd week -PE 3-4 weeks -bronchopnuemonia -after 1 month ->cardiovascular disease
complications
- neuropsychiatric diseases such as depression and dementia.
- dysphagia/dysphasia
- pneumonia
- cardiac arthymias
- GI bleeding due to stress ulcer
- bladder incontinence
- urinary tract infections secondary to catheterisation
- gait disturbance, falls and fractures
22
Q
ddx stroke
A
Thinking About Stroke Mimics Helps Me Consider Everything They Missed
- Todds paralysis
- Abscess
- Syncope
- Migraine with aura
- Hypertensive encephalopathy
- MS
- Conversion disorder
- Encephalitis
- Tumour
- Metabolic encephalopathy (hypoglycaemia)
23
Q
investigations stroke
A
Bedside:
Monitor O2 sats and RR. Hypoxia and hypercapnia worsen outcome.
Monitor blood glucose. Hypo/hyperglycaemia worsens outcome.
ECG
Consider echo
Bloods: CBC (platelets, anaemia) Coags Troponins EUCs
Imaging:
CT brain non con (most important. Ischaemic vs haemorrhagic)
- CT contrast (perfusion) gives estimation of penumbra
- CTA for visualisation of intracranial vessel, aortic arch
MRI
- Diffusion weighted superior to CT for detection of early infarct (particularly posterior fossa) but less widely available. As sensitive for haemorrhage.
- Infusion of gadolinium allows for perfusion study
- Area of discrepancy between diffusion and perfusion (no perfusion, fine diffusion) is penumbra
- MRA angiography
DSA
- gold standard for identifying stenosis and other pathologies such as anuerysm
- usually reserved for mechanical thrombectomy
Ultrasound
- duplex of carotids
- transcranial assessment of MCA, ACA, PCA flow
24
Q
internal carotid and ACA stroke syndrome
A
Internal carotid:
- often MCA like syndrome
- amorosus fugax common
ACA:
- contralateral hemiplegia, hemiparaesthesia of foot, leg and perineum
- impairment of gait
- bowel and bladder incontinence
- abulia, slowing of movement, latency (cingulate)
- left limb apraxia, left limb tactile aphasia (corpus)
25
MCA stroke syndromes
MCA:
proximal
-contralateral hemiplegia, hemiparaesthesia of face, upper limb and trunk
-dominant hemisphere = aphasia
-non dominant = hemineglect, anosognosia, constructional apraxia
-homonomous hemianopia
-defect in conjugate gaze, gaze preference to ipsilateral side
upper division:
- brachial syndrome
- brocas aphasia (with arm weakness = frontalopercular syndrome)
lower division:
- sparing of motor and sensory
- wernickes, conduction, transcortical sensory aphasia
- upper quadrantanopia
lenticulostriate:
- pure motor (posterior limb)
- genu = face with gradual involvement of upper limb then leg
- clumsy hand, dysarthria syndrome (genu and posterior limb)
26
PCA stroke syndromes
P1:
- Claude's with red nucleus (occulomotor palsy, contralateral ataxia)
- Weber's with involvement of cerebral peduncle (occulomotor with contralateral hemiplegia)
- Benedikt with subthalamus (occulomotor with hemiballismus)
- Pure sensory with involvement of thalamus
P2:
- cortical blindness without macular sparing, with or without intact awareness
- non-dominant = prosopagnosia
- visual hallucinations
- temporal lobe = memory problems, anomia
27
posterior circulation stroke syndromes
Medial medullary (anterior spinal):
- hypoglossal palsy ipsilateral
- contralateral hemiplegia (corticospinal) and hemiparaesthesia (medial lemniscus)
Lateral medullary (PICA):
- dysphagia and dysphonia (nucleus ambiguus)
- loss of pain and temp ipsilateral for face (spinal nucleus/tract of trigeminal) and contralateral for body (spinal lemniscus)
- ipsilateral horners (hypothalamospinal tract)
- vertigo and nystagmus (vestibular nucleus)
28
TBI ddx
- Extradural
- Subdural
- Subarachnoid
- Intraparenchymal haemorrhage
- Intraventricular haemorrhage (pial vessels)
- Axonal injury (diffuse or focal)
- Contusion
- Skull fracture (skull base)
- Mild TBI
29
types of cerebral hernias
- transtentorial
- subfalcine (cingulate)
- tonsilar
- transcalvarial
30
coma syndromes
Coma requirements
- involvement of both hemispheres
- or ascending reticular activating system in tegmentum of upper pons and mid brain
- Initially normal or Cheyne Stokes respiration, becoming more ataxic and eventually completely depressed
- With uncal herniation, CNIV is compressed giving dilated unresponsive ipsilateral pupil that eventually goes to mid position and fixed
- central tentorial will have bilateral mydriasis that goes to mid position and fixed
- Classically progression from localising to pain, withdrawing from pain, decorticate (diencephalon), decerebrate (red nucleus release of lateral vestibulospinal) and no motor response
- Compression of medulla leads to cardiorespiratory depression
31
causes CNIV palsy
INTIMA
- iatrogenic
- neoplasm
- trauma
- ischaemic (diabetic microvascular, infarct)
- migraine (opthalmoplegic)
- anaeursym (PICA)
32
prognosis extradural haemorrhage
Extradural:
| mortality 10%, 50% have good outcome, 30-40% have persistent disability, 5% have persistent vegetative state
33
sequelae TBI
- Second impact syndrome
- Post concussion syndrome (headache, nausea/vom, dizziness, cognitive impairment, neuropsych with change in mood)
- Post concussion headaches
- 2 fold increased risk of epilepsy
- Increased risk dementia
- Psychiatriac such as depression, mood change
- Sleep disturbance
- Vertigo
- Is some evidence for earlier mortality
34
pathophys ischaemic stroke
decrease BF --> increase anaerobic glycolysis and lactic acid production --> mitochondrial dysfunction and decrease in ATP production --> electrical failure due to inability to maintain ion gradient --> depolarisation --> glutamine release and NMDA receptor activation --> Ca and Na influx
Na --> increases intracellular water and oedema --> decreases glutamine uptake by astrocytes --> increased excitation
Ca --> permeablises mitchondrial membrane and worsens dysfunction --> decrease in ATP
NMDA --> increase nNOS and iNOS --> increased NO (free radical) --> direct damage to cellular components including DNA
Also inflammatory response --> release of MMP --> breakdown BBB --> oedema --> decrease BF/mass effect
End result = apoptosis (penumbra) or necrosis (infarct)
35
causes of seizures
SHITTEDD
- stroke
- haematoma (epidural/subdural)
- infection (meningitis/encephalitis/abscess)
- TBI
- Tumour
- encephalopathy (electrolyte, glucose, uraemia, ammonia)
- drugs and alcohol
- degenerative (alzheimers)
36
hx and exam seizures
```
HxPC
-description of event
-may require collateral
-abrupt onset, lasts less than 5 mins
-loss of awareness/movements
-injuries
-post ictal
-triggers (MEDICATION COMPLIANCE!)
PMHx
-past events
-prompt by asking about myoclonus, hallucinations
-epilepsy disorders
-risk factors/causes
FHx
-epilepsy
Psychosocial
-drugs and alcohol
-progression
-driving
-ADLs
```
```
Exam:
neurological
-localising symptoms
assess orientation
tongue biting
-specific (uncommon in psychogenic)
```
37
seizure investigations
Blood glucose
ECG
FBC
EUC and CMP
Toxicology screen (if indicated)
bHCG if female (treatment)
```
Lumbar puncture (if infection suspected)
EEG (relatively low sensitivity)
-if still confused, as inpatient
-otherwise can be done as outpatient
MRI brain
```
Consider:
serum prolactin (limited utility)
-needs to be performed within 20 mins of seizure
-useful in identifying focal with impaired awareness
-distinguishing psychogenic from real
