Neuro Flashcards
(45 cards)
Causes of Stroke
Ischaemic- emboli or atheroscleroti
Hemorrhagic- Intracerebral haemorrhage
SAH
SDH
EDH
Venous
RFs for CVA
Smoking HTN dm af Previous TIA Carotid artery stneosis FH OCP ETOH Obese
Bamford Classication
Lacunar stroke= any of Pure motor hemiparesis Pure sensory hemiparesis Ataxic hemiparesis Sensori motor stroke
TACI (Total anterior circulation infarct)-
3 or 3
1) Higher cerbreal dysfunction
2) Homonymous field defet
3) Ipsilateral motor defect of two regions (of face, arms and legs)
PACI (Partial anterior ciruclation infarct)
2 or 3
Posterior circulation infarct
One of….
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
Difference between ACA and MCA strokes
ACA= Affects legs over arms- more likely to have urinary incontinence
MCA= Weakness of arm and face over legs
Expressive or receptive dysphasia if dominent hemisphere
Quadrantiopia depending if parietal (floor) or temporal (sky) lobe affected
Other cortical signs including
a) Sensory cortical impairment- 2 point discrimination, unable to recognise from touch and agraphaesthsia
b) Dominent parietal lobe- sensory cortical features plus auditory agnosia, Gerstmann syndrome (inability to calculate, read or write, finger agnosia and loss of left-right discrimination)
c) Non dominant parietal lobe- hemi neglect, apraxias (e.g in dressing or gait)
(View like structure of blood supply to brain!)
Posterior Circulation infarct syndromes
1) PICA syndrome (Wallenberg's) Ipsilateral pain and pinbrick impairment to face and contralateral trunk and extremity pain and pinprick Dysphagia hoarsenss and logg of gag Vertigo,nystagmus Ipislateral cerebellar signs
Aka CN 8-10 and cerbellar
2) AICA syndrome (Lateral pontine- Unwellenberg’s)
Ipsilateral sensory impariment of face and contralateral trunk
Paralysis of ipsilatreal muscle sof mastication and paralysis of face (LMN)
ipsilateral hemiataxia
So affects CN 5+7
3) PCA occlusion- contralateral homonymous hemianopia with macular sparing
Contrlateral pain and temp loss
Memory deficits
Cortical blindness and hemineglect
4) Weber’s syndrome (3rd nerve palsy and contralateral hemiplegia due to infarct of medial midbrain
Investigation of stroke
Identify timing of stroke regarding thrombolysis
Baseline obs, CBG, BP and 12 lead EG.
Baseline bloods- FBC, Clotting, TFTs, LFTs and ANA
Hba1c, Lipid profile
CT head- may do CT angio if considering thrombolysis or thrombectomy
Alongside this- SALT MRI head 24 hour tape TTE Carotid dopplers
If young want to investigate for thrombophilias and inflammatory causes
Management
If caught in first 4.5 hours then thrombolysis
May also consider thrombectomy
CI to thombolysis= previous ICH Active internal bleeding or previous GI bleed, liver disease or varices. Surgery in last 14 days BP >185/110 Stroke or head injury in last 3 months.
If non haemorrhagic then want to give loading aspirin- switch to clopidogrel or DOAC depending on evidene of AF
Start statin and treat BP and DM if diagnoses
If Carotid artery >70% stenosed then carotid endarterectomy.
SAH summary
RFs- FH, APCKD, Ehlers Danlos Marfan's Smoking HTN Drugs e.g cocain IE with mycotic aneurysm
Classical features
Complications- Vasospasm most often around 4-10 days. Treat with Mifedipine. Hydrocephalus- Rebleeding Seizures Pulmonary oedema Cardiac arrythmias Hyponatraemia (SIADH or salt wasting)
Ddx of stroke
SOL e.g tumour or abscess or parasite
Viral encephalitis
Neuroinflammation- MS, neurosaroid, Bechet’s
Todd’s paresis
Migraine
Stroke mimic on old stroke when otherwise unwell
Multiple Sclerosis Clinical features
Can affect nearly any part of the CNS
Optic neuritis- pain on movement, reduced acuity and olour desaturation
Diplopia due to INO
Spinal cord syndrome- urinary/bowel dysfunction, sensory dysfunction or paraparesis
Motor involvement later in disease with weakness and spasticity
Cerebellar signs
Dysarthria, vertigo
Lhemmitte’s sign- electricla sensation from neck to limps on flexion
Uhthoff’s phenomen- worsening of symptoms on rise in body temp)
Classification
Relapsing-remitting MS- 85%
Secondary progressive MS- can develop from relapsing remiting
Primary progressive MS
Investigations in MS
MRI head and Spine
Basic blood tests to rule out Ddx
Visual and auditory evoked potential to demonstrate old lesions
CSF may show oligoclonal bands
Management of MS
Acute episode- IV methyprednisolone
Screen and treat any systemic infections
Get neurologist involved for diagnosis and management
Symptomatic management- MDT approach= PT/OT/SALT
Antispastmodics
LT catheter or intermittent self catherisation
Laxatives
Treat pain, swallow, depression, sexual dysfunction
Disease modifying therapy- Beta interferon and glatiramer can be used (SEs- flu like symptoms, AI hepatitis, and failure to be efficacious)
Natalizumab- mab against adhesion molecule on T cell
Alemtuzumab Anti cd52
Fingelomod- oral agent for highly active mS
All mainly used RRMS
Neuromyeltitis optica
Demyelination of spinal cord and optic nerves
Have a more extensive lesion sthen in MS and often extends over 3 vertebral segments.
Due to Antibody against aquaporin 4
Responds to IV iG and plasma exchange in short term event
Steroids and immunosuppression in long term
Parkinson’s disease signs
Walking aids/anti parkinsons medications Hypomimic facies, siallorhoea, Classic cait, reduced arm swing and difficulty turning Asymmetricla tremor, worse on distraction Bradykinesia Lead pipe rigiity and cogwheel rigidity Quiet monotonous speech Micrographia Impaired sense of smell
Causes of Parkinsonism
Idiopathic PD Drug induced (neuro-epileptis and anti emetics) Parkinson's plus- Progressive suprnuclear palsy, MSA and corticobasal degeneration Dementia wiht Lewy bodies TOxins- MPTP, manganese Wilson's disease Post trauma VASCULAR PARKINSONISM
Treatment of Parkinson’s disease
Involve neurology team and Parkinson’s nursing team
L-dopa Dopamine agonists Monamine oxidases inhibitors COMT inhibitors Amantadine Anticholinergics
Cerebellar disease Symptoms
DANISH
Dysdiadochokinesis- Ataxia Nystagmus Intention tremor Staccato speech Hypotonia/hyporeflexia
Will also have rebound phenomenon and ataxia on gait and truncal
Causes of Cerebellar disease
Demyelination- MS Alcohol SOL Parneoplastic Stroke (Ischaemic) Hypothyroidism Drugs e.g phenytoin Metabolic- B12 or copper (Wilson's)
Genetic causes include spinocerebellar ataxia and fredrich’s ataxia
Spinocerebellar ataxia
Large range of subtypes of spinocerebellar ataxias
AD and can have extrapyrimidal sings, peripheral neuropathy and opthalmoplegia
Fredrich’s ataxia- has peripheral neuropathy, spasticit, diabetes and deafness. Wheelchair bound often
Demonstrate anticipation!
ATAXIA TELANGIECTASIS- SKIN AND EYE TELANGIECTASIA AND DYTONIA. ar INHERITENCE
Spinal Cord disorders- clinical findings
Spastic gait
Spasticity in lower limbs (increased tone) and clone
Reduced power- (Extensors worse then flexors in arms, flexors worse then extensors in legs)
Hyperreflexia
Sensory level above L1
Catheter in situ
Spinal surgery scars
Classification of spinal cord disease
1) Vascular- Occurs within minutes.
Such as Anterior spinal artery infarction or AVM
Anterior spinal infarction will spare dorsal column sensation
2) Compressive- Hours to days. Often asymmetrical.
Predominantly motor but can affect sensory systems
Include- Degenerative disease- e.g disc herniation
Malginancy- both mets, and intermedullary or extramedullary
Trauma
Abscess
3) Infective- Hours
Often more painful and associated fevers
Can be bacterial- e.g Staph, strep, TB
Or viral, HIV, enterovirus, Herpes and HTLV
4) Inflammatory- Hours to days
Such as due to MS, SLE, sarcoid or vasculitis
5) Nutritional/metabolic- Days to weeks/months
Such as B12 decifiency or copper deficiency
Associated with loss of dorsal column sensation
6) Neurodegenerative and congenital-
Several different conditions within these. Occur over months-years
Key example is hereditary spastic paraperesis- have increased tone and spasticity with reflexes but persevered power
Can also occur in Fredrich;’s ataxia and spinocerebellar disease.
Investigations
MRI spine
Blood tests and markers for infection/vasculitis if concerned
Vit B12 too and HIV test
MR angiogram if thinking vascular cause.
If thinking MS then concurrent visual and auditory evoked potentials for previous episodes.
Bulbar and pseudobulbar palsy
To examine use- Bbb for lips, ttt for tongue, kkk for palate
Bulbar palsy is LMN lesion- Have nasal speech and fasciculations and wasting of the goneu
Caused by MND , myasthenia gravis, myopathy
Pseudobulbar palsy is UMN lesion-
Have spastic hoarse voice and slow tongue
Linked to brisk reflexes in jaw
Causes MND, MS and brainstem stroke