Neuro Flashcards
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
Causes of Mixed UMN and LMN signs
1) Cervical radiculopathy
2) MND
3) Subacute degenration of the cord
4) Syringomyelia
5) Conus meddlaris compression- as per classic cauda equina. Will have sphincter disturbance, sensory level and weakness assocaited
Plus saddle anaesthesia.
Signs of cervical radiculopathy
Wasting of arm muscles- if C5-C6 then of biceps and supinators
If c8-t1 then small msucles of hands
Brisk reflexes belown lesion
Pain localised to neck in radicular pattern
Sensory loss localised to radicular patten
Motor Neurone disease- signs and management
Mixed picture Will can have reduced or spastic tone Reduced power Brisk or absent reflexes Fasciculations- diagnostic
Sensation will remain intact
Subtypes include- Amyotrophic lateral sclrosis- Classic picture affects UMN and LMN of limbs and bulbar system
If only bulbar then is progressive bulbar palsy
primary lateral sclerosis- Only UMN signs
Progressive muscular atrophy- only LMN signs
Dx- is by EMG demonstrating widespread denervation
Mx- Supportive
MDT in put for symptom control and optomisation
PT/OT/SALT- may need PEG
Riluzole will prolong lifespan by 3 months
May need NIV if T2RF due to neuromusclar weakness
Syringomyelia
Fluid filled cyst in central spinal cord- linked to tumours and arnold chiari malformation
Signs - Loss of pain and temperature sensory loss but but not touch or vibration or position.
Described as cape like as affects arms and thorax but not legs
May have scars from burns and cuts not recognised
Wasting and weakness of small muscles of hands
Brisk lower limb reflexes and upgoing plantars
May have Horner’s syndrome
Subacute degeneration of the cord
Signs
Brisk knee jerks, absent ankles
Symmetrical sensory neuropathy. May be burning and lose touch, vibration and potision sense
Reduced lower limb power
Positive romberg’s sign
May be anaemic
May have optic atropy or dementia due to B12 deficinecy
Check abdomen for splenomegaly or previos surgery- e.g in crohn’s
Causes- Poor oral intake, Pernicious anaemia, ETOH intake and nitrous oxide abuse
Causes of facial nerve palsy
UMN lesion= spares forehead due to bilateral innervation
LMN lesion= forehead will also be paralysed
Unilateral= Bell's Palsy Ramsey Hunt syndrome Stroke Demyelination SOL (CPA lesion) Nerve infiltration e.g sarcoid
Bilateral= Bilateral Bell's palsy Sarcoid AI e.g GBS Muscular dystrophy esuch as myotonic or fascioscapulohumeral Infection such as Lyme
Peripheral nerve root terms
Polyneuropathy- diffuse involvement of peripheral nerves
Mononeuropathy- involves on nerve
Mononeuritis multiplex- focal involvement of 2 or more neves.
Rsdiculopsrhy- single spinal nerve root
Plexopathy- involvement of brachial or lumbosacral plexus.
Radiculopathy- characteristics and causes.
Burning tingling pain radiating down limb
Weakness and senroy loss in myotomal distribution
Loss of reflexes and moeot strength
Chronic rsdiculopsrhy- can result in atrophy and fasciculations.
T1 radiculopathy- causes Horner’s
Causes- Disc herniation Cervical/lumbar spondylosis Spinal stenosis Compression by tumour Inflammation Infections.
Radiculopathy- characteristics and causes.
Burning tingling pain radiating down limb
Weakness and senroy loss in myotomal distribution
Loss of reflexes and moeot strength
Chronic rsdiculopsrhy- can result in atrophy and fasciculations.
T1 radiculopathy- causes Horner’s
Causes- Disc herniation Cervical/lumbar spondylosis Spinal stenosis Compression by tumour Inflammation Infections.
Brachial plexopathy
Muscle weakness and atrophy from c5-t1
Reduced tendon reflezesensory loss often of axillary nerve.
Causes neuralgic amyotrophy Neoplastic eg breast and lung cancer Radiation induced Thoracic outlet syndrome Iatrogenic after surgery
NB c8 lesion will cause weakness of flexor policcis Longus and extensor pollicis brevis whi h ulnar lesion won’t do
Median Nerve palsy
Supplies LOAF, long finger flexors and sensation to lateral 2/3rds of palm and 3.5 fingers.
Causes
Carpel tunnel syndrome linked to other pathologies E.G Ra and acromegaly and pregnenacy And diabetes and hypothyroid
Trauma
Surgical injury
Clinical signs Wasting of thenar eminence Weakness of APB, oppons pollicis and lumbrical. Sensory loss over relaxsnf region. Provoked by Tinel's and phalens test.
Ulnar nerve palsy
Signs wasting of dorsal interossei Wasting of hypothenar eminence Clawing of 4-5th fingers Generalized weakness of hannd Sensoey impairment oflvsd little and ulnar ring finger
Innervates hypothenar muscles Medial 2 lumbrical Interossei Adductor pollicis Medial wrist flexors
Causes Compression at the elbow e.g bone, prolonged elbow flexion and op compression Bony deformity at evlow- fractures and RA and pagets Idiopathic Variable anatomy Diabetes Vasculitis Leprosy
Radial nerve palsy
Signs- weakness of wrist extension
Weaknes of finger extension.
If wrist is pasicly extended CNA then straighten fingers
Weakness of finger abduction and adductio.
If weakness of tricep relfex think lesion in axilla or c7 radiculopsrhy-
Causes- injury at elbow by fracture of dislocation
At humeral shaft fracture
At axilla due to traumatic compression fromx rutches or Saturday night palsy.
NB an intact trcieps reflex suggests lesion below spiral groove.
Common peroneal nerve palsy
Signs- High stepping gait
Wasting of muscle on lateral lower leg
Weakness of dorsiflexion and eversion of foot
Sensory impairment over anterolateral aspect of lower leg
Causes- compression Direct trauma Diabetes Mononeuritis multiplex Leprosy will have palpable thickening of nerve.
Polyneuropathies causes
Sensori-Motor= Diabetes Nutritional (B12) deficiency) ETOH Drugs e.g isoniazid, metronidazole, chemotherapy agents and phenytoin Hypothyroidism, renal failure Infections e.g HIV and leprosy and syphillis Vasculitis Hereditary- Charcot marie tooth disease
Motor predominence= Inflammatory e.g AIDP, CIDP, MGUS associated.
Lead poisoing
Diabetic amyitrophy
Inherited e.g spinal muscular atrophy
Sensory- Paraneoplastic, Fredrich’s ataxia, chemotherapy
Polyneuropathy signs
Glove and stocking sensory impairment
Muscular atrophy of affected areas
Reduced reflexes
Autonomic dysfunction with postural hypotension, impotence, GI changes and urinary inontinence.
Small fibre neuropathy affects temp and pin prick
Large fibre affects soft touch, vibration and proprioception
But often both affected
Polyneuropathy investigations
History and complete neurological exam (All 3 parts)
Urine dip
Bloods for FBC, ESR, B12, Folate, HBa1c, tftS, u+E and LFTs
Can then move onto nerve conduction studies and EMG to characterise affected nerves Vasculitis screen Eletrophoresis CXR HIV
May do antineuronal antiboodies eg anti hu and anti Yo for paraneoplastic
CT-CAP for cause if above all negative.
Fredrich’s ataxia
AR progressive ataxia. Most common inheritied ataxia in UK.
Inherited with Triplet repeat due to mutation on fraxin gene.
Is a spinocerebellar disese- symptoms hinted in the name!
Affects dorsal column
Neurologically develop a form of spastic paraparesis
Often have a wheelchair or walking aid present.
Will have increased tone
Reduced power in pyramidil distribution.
Absent ankle reflexes but upgoing plantars/clonus is characteristic
Also reduced coordination of hands and legs
And cerebellar speech
Sensation- reduced dosral column
Other features of Fredrich's ataxia Pes cavus Kyphoscoliosis Deafness with hearing aids T1DM- so look for CBG pin pricks Arrythmias and hypertrophic cardiomyopathy - so pacemaker may be present
Ix to cover neurological symptoms, risk fo daiebtes and cardiovascular risk too
Management will need to be MDT with relavent specialists and allied health professionals involved.
Hereditary sensory and motor neuropathy
AKA
Charcot Marie Tooth Syndrome
In contrast to Fredrich’s ataxia this is a polyneuropathy!
Is AD inheritance
Subtypes include demyelinating and axonal.
On examination will find;
Wasting of distal lower limb but preserved thigh muscles (causign inverted champagne bottle apperance)
Pes cavus
Weakness in ankle dorsiflexion and toe extension
Variable degree of stocking distrubution sensory loss
Gait will be high stepping
Also wasting of hadn muscles
Palpable lateral popliteal nerve
Causes of flaccid paralysis
Split into sections of nerves
TO guide presentation if not sure and also to help guide Ddx
Nerve foot- plexus- nerve- NMJ- Muscle
Nerve root= MND or polio
In between have cauda equina and compression
Plexus= Trauma, tumour or abscess affecting lumosarcral plexus but note often unilateral
Nerve- Several causes Inflammation e.g GBS or CIDP Infections e.g HIV Toxins- Lead Metabolic- Porphyria and diabetic neuropathy Congenital- Charcot Marie Tooth
NMJ- Myasthenia gravia
Botulinism
Organophospahte poisoning
Muscle-Congenital myopathy- Myotonic dystrophy, Duchenne/becker's Inflammtory- Poly/dermomyositis Endocrine- Hypothyroid, Cushing's ETOH Electrolyte disurbances
Causes of spastic paralysis
See spinal diseases. These show rough guide
Aka- break down is
1) MS
2) Cord compression (Sensory level)
3) Vascular cord injury (Sensory level)
4) Trauma
5) Cerbral palsy
Also can think of Fredrich’s ataxia
Hereditary spastic paraparesis
Tropical spastic parapresis
And also syringomyelia
