Neuroscience Flashcards
Name 5 symptoms of Bell’s Palsy
Unilateral Facial Weakness Ear Numbness Ear Pain Decreased Taste Hypersensitivity to sounds (Hyperacusis)
Name 2 risk factors for Bell’s Palsy
Pregnancy x3
Diabetes x5
Name 5 general symptoms of a 7th Nerve Palsy
Dry eyes Unilateral sagging of the mouth Drooling Food trapped between gum and cheek Speech difficulty
Name 4 possible complications of Bell’s Palsy
Dry eyes
Sagging eyelids
Synkinesis
Crocodile tears
What is the common and most benign CNS tumour
Astrocytoma
What is the most aggressive CNS tumour
Glioblastoma
What is the ideal way to investigate CNS tumours
CT head is 1st Line
MRI actually has higher sensitivity
What is the cardinal presentation of Cluster Headaches
Unilateral excruciating orbital/temporal pain - Usually nocturnal
Name 4 risk factors for Cluster Headaches
Male sex
Head injury
Smoking
Alcohol - Common trigger
What are the possible associated symptoms of Cluster Headaches
Over stimulation of PNS Lacrimation Rhinorrhoea Miosis/Ptosis Facial Oedema Agitation
N+V
Phono/Photophobia
What are the diagnostic criteria for Cluster Headaches
International headache society-3b criteria
A - 5 headaches + satisfying B-E
B - Excruciating unilateral orbital/temporal pain lasting 15 - 180 minutes if left untreated.
C - At least 1 PNS associated symptom
D - Multiple headaches occurring a minimum of 1 every other day lasting 15-180 minutes each. Remission periods between attacks
E - Not attributed to another disorder
What are the 4 main subtypes of Dementia
Alzheimer’s (50%) -
Vascular (25%) - Cumulative effect of many small strokes
Lewy body (15%) - Fluctuating cognitive impairment, detailed visual hallucinations, later parkinsonism
Fronto-temporal (5%) - Executive impairment and personality changes
Parkinson’s disease dementia - Parkinson’s disease predates dementia
What are causes of reversible Dementia and what are investigations to test for these
Hypothyroidism - High TSH B12 and folate deficiencies Thiamine deficiency Hypocalcaemia Subdural haematoma - CT/MRI Normal pressure hydrocephalus - CT/MRI
Delineate subtypes - Functional Imaging
EEG
What are symptoms of Alzheimer’s Dementia
All dementias: Memory loss
Confusion, Apraxia, Aphasia
Later disease: Wandering, Disorientation, Psychiatric and Behavioural problems
How can you differentiate Alzheimer’s Dementia from the main other types
Vascular: Stepwise decline after a vascular event
Lewy body: Fluctuating levels of consciousness, hallucinations, sleep disorders, falls and parkinsonian features
Parkinson’s disease dementia: Parkinson’s disease predates dementia
Fronto-temporal: Behavioural changes (Disinhibition or apathy) and language disturbances
What are the main causes of Encephalitis
Viruses are the main cause - Most commonly HSV infection. Other viruses include arbovirus worldwide
Name 4 risk factors for Encephalitis
Immunodeficiency
Body fluid exposure
Organ transplantation
Bites
What are the signs and symptoms in Encephalitis
Fever
Headache
Altered mental state
Seizures
+ Other meningitis symptoms (Neck stiffness, Vomting)
Focal neurological
Raised ICP
Psychiatric symptoms
What are the main investigation findings of Encephalitis
Bloods - Blood cultures
CT - Do before LP
LP - Increased Proteins, Lymphocytes and decreased glucose. Send CSF for viral PCR
EEG - Diffuse abnormalities
Name 6 causes of Epilepsy
Most idiopathic
Developmental Head injury Cranial surgery - Cortical scarring Space occupying lesion Cerebrovascular event Genetic disease
What is the major cause of Extradural haemorrhage
Trauma to the pterion causing middle meningeal artery damage
What are the early and late signs of Extradural haemorrhages
Early signs
Headache
Immediate fluctuating consciousness before a lucid interval (6-8hrs)
Late signs Rapid deterioration after regaining consciousness (Falling GCS) Bradycardia + Hypertension (Rising ICP) Vomiting Confusion Seizures Hemiparesis + UMN Reflexes
Latest Ipsilateral pupil dilation Bilateral limb weakness Irregular breathing Coma + Death (Respiratory arrest)
What are the main investigation findings in Extradural haemorrhages
Biconvex opacity + Midline shift + Brainstem herniation (Poor prognosis) - CT
XR - Skull fracture
NO LP!!!
What are typical triggers of Guillain-Barré syndrome
A few weeks after an infection a symmetrical ascending muscle weakness starts.
Triggered after: Campylobacter jejuni, CMV, mycoplasma, Zoster, HIV, EBV, vaccinations.
What is the cause of Guillain-Barré syndrome
Due to autoantibodies attacking myelin sheath and schwaan cells.
What are the possible signs and symptoms of Guillain-Barré syndrome
Due to autoantibodies attacking myelin sheath and schwaan cells.
Paraesthesia’s in hands and feet frequently precede onset of weakness
Back and leg pain in most cases
Proximal nerves mainly affected - Trunk and respiratory muscles then cranial nerves
Areflexia
Potential autoimmune dysfunction - Sweating, Tachycardia, Arrhythmias, Hypertension
What are the 4 definitive signs of Guillain-Barré syndrome
Motor difficulty
Areflexia
Paraesthesia without objective sensory loss
CSF albumin with no cellular reaction
What are the main 4 investigative findings in Guillain-Barré syndrome
Slow conduction - Nerve conduction studies
CSF high protein but normal WCC - LP
Monitor FVC every 4 hours and if there is sufficient deterioration mechanically ventilate.
What are the signs of Horner’s syndrome
Unilateral: Miosis Ptosis Anhidrosis \+ Enopthalmos
Name 3 broad causes of Horner’s syndrome
Interruption of faces sympathetic supply at:
The brainstem: Demyelination -MS, Vascular disease - Stroke, Carotid artery dissection
The cord: Syringomyelia
Thoracic outlet: Pancoast tumour
Name 3 potential investigations to investigate Horner’s syndrome
Investigating cause:
CXR: Apical lung tumour
CT/MRI: Cerebrovascular accident
CT angio: Dissection
What is the time from diagnosis to death in Huntington’s disease
20 years max
It is slow progressing and it is certain death
What are the symptoms seen in the prodromal phase of Huntington’s disease
Irritability
Depression
Incoordination
What are the definitive features of late Huntington’s disease
Chorea
Dementia
Fits
Death
What part of the brain degenerates in Huntington’s disease
Striatum and cortex
What are the main signs and symptoms of Migraines
Potential aura Throbbing/pulsatile pain Worsening with movement Phono/Photophobia N+V Usually unilateral
What are common triggers for Migraines
CHOCOLATE
Chocolate Hangovers Orgasms Caffeine Oral contraceptives Lie-ins Alcohol Travel Exercise
How are Migraines diagnosed
Clinically
A least 5 headaches lasting 4-72hrs + N+V/Phono/Photophobia +2 of Unilateral/Pulsating/ Impairs routine activity
What are prophylactic treatments for Migraines
BB - Propranolol
Anti-convulsant - Topiramate
TCA - Amitriptyline
What are the treatments for Migraines during attacks
Mild
NSAID
Paracetamol
Paracetamol + Aspirin/Caffeine
Severe Triptans + NSAID Ergot alkaloids + NSAID Corticosteroids + NSAID Butalbital-containing compound + NSAID
All with antiemetics
What are the 4 different Motor neurone diseases
ALS - Amyotrophic lateral sclerosis - Motor cortex + Anterior horn = UMN + LMN Signs - Worse prognosis if bulbar onset
Progressive bulbar palsy - CN9-12
Progressive muscular atrophy - Anterior horn = LMN
Primary lateral sclerosis - UMN signs
How can we distinguish between Motor neurone diseases and demyelinating diseases
There is no sensory loss or sphincter disturbance in MNDs
How can we distinguish between Motor neurone diseases and Myasthenia Gravis
MND never affects eye movements
What are the UMN, LMN and bulbar signs of Motor neurone diseases
Typical signs: Spastic gait with foot-drop +/- Proximal myopathy, Weak grip and shoulder abduction or aspiration pneumonia
UMN: Spasticity, Hyper-reflexia, Upgoing plantars
LMN: Wasting, fasciculations
Bulbar: Speech or swelling affected
What is the usual progression of ALS
Asymmetrical limb involvement in most cases though it can also start with bulbar signs sometimes or respiratory signs rarely
How would you investigate suspected Motor neurone disease
MRI - Structural causes
LP - Inflammatory causes
EMG - Denervation
What is the common diagnostic description for Multiple sclerosis
Episodic neurological dysfunction in at least 2 areas of the CNS separated by space and time
What are the most common presentations of Multiple sclerosis
Usually monosymptomatic
20% Unilateral optic neuritis (pain on movement and a rapid decline in central vision)
Corticospinal tract and bladder involvement (Autonomic) are common
Foot-drop or spastic paraplegia
Uhthoff’s sign: Symptoms may worsen with heat
Lhermitte’s sign: An electrical sensation that runs down the back and into the limbs when the neck is flexed
Internuclear
Ophthalmoplegia - Lesion in the MLF
What are the different types of presentations found in Multiple sclerosis
Motor syndromes
Brainstem syndromes
Cerebellar syndromes (ataxia), Sensory syndromes
What are investigative findings in Multiple sclerosis
Hyper-intensities + demyelinating lesions in the CNS - white matter - MRI
Immunoglobulin bands - CSF PCR
What is the cause of Myasthenia Gravis
It is caused by autoimmune destruction of postsynaptic NMJ nAChR and the associate proteins (Namely Muscle specific tyrosine kinase)
What are the 3 forms of Myasthenia Gravis and what are their associated symptoms
Ocular: Ptosis, Diplopia
Oropharyngeal: Dysarthria, Dysphagia, Facial paresis
Generalised: Proximal limb weakness (Worse in evening), Dyspnoea
Generally better with rest and worse with use.
50-60% that present with purely ocular will develop generalised in 1-2 years
Which groups of people are usually affected by Myasthenia Gravis
<50 Women +/- Rheumatoid Hx +/- Thymic hyperplasia
>50 Men +/- Thymic atrophy/tumour
What are the investigative results of Myasthenia Gravis
- Serum AChR antibodies analysis
- Muscle specific tyrosine kinase (MuSK) antibodies
- Serial PFTs
What are the 3 symptoms defining Parkinsonism
Tremor
Hypertonia
Bradykinesia
What are the main symptoms of Parkinson’s disease
Signs always worse on 1 side.
Parkinsonism+
Sleep disturbance
Anosmia
Autonomic dysfunction (Postural Hypotension, Constipation, Urinary frequency)
Neuropsychiatric dysfunction (Depression, Dementia, Psychosis)
How may one investigate atypical Parkinson’s disease
Dopaminergic agent trial - Levodopa
What is Spinal cord compression
Compression of the bloody supply, CSF spaces or cord
What are the causes of Spinal cord compression
Mainly trauma
Intervertebral disc disease (Herniation)
Vertebral compression - Bone diseases/Steroids
Malignancy
Infection
What are the signs and symptoms of Spinal cord compression
Sensory (3): Altered sensations, hemisensory loss and pain (Common PC)
Motor (3): Hemi/Para/Tetraplegia or Hemi/Para/Tetraparesis (sparing face)
Autonomic (7): Constipation, Urinary retention, Dizziness, Hypothermia, ED, Abdominal pain, Syncope
What are the investigative findings of Spinal cord compression
Disc displacement, epidural enhancement mass effect - MRI
Decreased disc space height - XR
Bony fragments + tumour expansion
What is Radicuolpathy
This is pathology arising from the nerve root
Usually due to mechanical compression
What are the cause of Radiculopathy
Main causes are intervertebral disc disease and osteoarthritis
Other causes include trauma, Facet joint degeneration, ligamentous hypertrophy, spondylolisthesis
Rare causes include radiation, DM and malignancy
RFs: Obesity, Poor posture, pregnancy
What are signs and symptoms of Radiculopathy
Sensory (5): Altered sensation, Tingling, Numbness, Shooting pain. Sharp pain (movement)
Motor: Hypo-reflexia, Weakness
What are the investigations used in Radiculopathy
The same as Spinal cord compression +
EMG - Motor
Nerve conduction studies - Sensory
What are the risk factors for Subarachnoid haemorrhage
Smoking Hypertension Alcohol Ehlers-Danlos Marfans Polycystic kidney disease Neurofibromatosis Type 1
What are the signs and symptoms of a Subarachnoid haemorrhage
Worst headache of life
Photophobia
LOC
Potential 3rd Nerve Palsy
N&V
Meningism
What are the investigative findings in Subarachnoid haemorrhage
Hyperdense areas in CT
Xanthochromia in the LP
Troponin I - Elevated
What are the cause of Subdural haemorrhage
Trauma
Venous
Arteriovenous abnormalities or other systemic bleeding disorders
Anticoagulant use
What are the signs and symptoms of a Subdural haemorrhage
Headache
N&V
Reduced GCS
Confusion
LOC Seizure Incontinence Neurological changes Localised weakness Oto/Rhinorrhoea
What are the investigative findings in Subdural haemorrhage
Banana shaped mass + Midline shift + Brainstem herniation on CT
XR
No LP
Outline the treatment algorithm for Subdural haemorrhage
Small <1cm diameter or Midline shift of <5mm:
1st Observational; follow up imaging
+ Prophylactic anti-epileptic (Phenytoin)
A Correction of coagulopathy
Large:
1st Surgery + Everything else
What is the most important complication to consider when treating Subdural haemorrhage
Epilepsy!! Hence prophylactic anti-epileptics are given
Coma
Neurological defects
Stroke
What is the character of Tension headaches
Generalised head pain like a tight band around the head with normal neurological examination
Potential
Facial muscle tenderness
What is the treatment for Tension headaches
Acute - Simple analgesic
Chronic - Antidepressant (Amitriptyline)/Muscle relaxant (Tizanidine)
What is the main complication of Tension headaches
Peptic ulcer
What is the cause of Trigeminal neuralgia
80-90% due to nerve compression of 1 or more branches of the trigeminal nerve.
Demyelinating disease - e.g. MS
What are the main symptoms of Trigeminal neuralgia
Sudden episodes of sharp, stabbing, intense pain lasting up to 2 minutes potentially with a constant component of facial pain.
What are common triggers for Trigeminal neuralgia
Tooth brushing
Eating
Cold
Touch
How is Trigeminal neuralgia diagnosed
It is a clinical diagnosis but one may perform:
Trigeminal reflex testing
MRI or
Intraoral XR
Who is more susceptible to Wernicke’s encephalopathy
It is caused by a deficiency in thiamine leading to focal areas of brain damage
Chronic Alcoholism Eating disorders Malnutrition Prolonged vomiting (e.g. Chemo, GI malignancy, Hyperemesis gravidarum) AIDS Thyrotoxicosis
What are the signs and symptoms of Wernicke’s encephalopathy
Triad:
Confusion
Ataxia
Ophthalmoplegia (Nystagmus, Lateral rectus or conjugate gaze palsies)
Memory disturbances Hypotension Hypothermia Reduced consciousness Hallucinations
Korsakoff’s psychosis = Deterioration leading to:
Amnesia &
Confabulation
How is Wernicke’s encephalopathy diagnosed
Diagnosis is mainly based on history and examination
Therapeutic trial of parenteral thiamine - Clinical response
Blood alcohol level
Blood thiamine and its metabolites
What is the normal ICP in adults
<15mmHg
What are causes of Raised ICP
Tumour Haemorrhage Hydrocephalus Cerebral oedema Head injury Infection: Meningitis, encephalitis, brain abscess Status epilepticus
What are the signs and symptoms of Raised ICP
Headaches (Worse on coughing, leaning forward)
Vomiting
Altered GCS
Cushings response: Bradycardia, hypertension and irregular breathing (Cheyne-Stokes)
Pupil changes - Constriction then later dilation
Decreased visual acuity, peripheral field loss
Papilloedema is an unreliable sign - Venous pulsation at the disc may be absent
What are the appropriate investigations for Raised ICP
U&Es, FBC, LFT, Glucose, Serum osmolality, clotting, blood culture.
Toxicology screen
CXR - Any source of infection?
CT head
LP if safe (Measure the opening pressure)
What is Neurofibromatosis
This is an autosomal dominant genetic disorder affecting cells of neural crest origin resulting in the development of multiple neurocutaneous tumours
What the different classifications of Neurofibromatosis and what are the definitive features of each
Type 1 (von Recklinghausen's disease): Peripheral and spinal neurofibromas Multiple cafe au lait spots Freckling axillary/inguinal Optic nerve glioma Lisch nodules Skeletal deformities Phaechromocytomas Renal artery stenosis
Type 2: Schwannomas Meningiomas Gliomas Cataracts
What are the presenting symptoms of Neurofibromatosis
FHx
Type 1: Skin lesions Learning difficulties Headaches Disturbed vision (due to optic gliomas) Precocious puberty
Type 2: Hearing loss - Sensorineural Tinnitus Balance problems Headache Facial pain Facial numbness
What are the appropriate investigations for Neurofibromatosis
Ophthalmological assessment Audiometry MRI for tumours Skull XR - Sphenoid dysplasia in NF1 Genetic testing NF TSG Mutations
What is hydrocephalus and how can it be classified
It is enlargement of the ventricular system
Obstructive (Non-communicating) or Non-obstructive (Communicating)
There is also hydrocephalus ex vacuo = Apparent enlargement of the ventricles as a compensatory change due to brain atrophy
What are obstructive and non-obstructive causes of CSF accumulation
Obstructive: Impaired outflow:
Lesion of 3rd or 4th ventricle or cerebral aqueduct
Posterior fossa lesions compressing the 4th ventricle
Cerebral aqueduc stenosis
Non-obstructive: Impaired CSF reabsorption into subarachnoid villi:
Tumour
Meningitis
Normal pressure hydrocephalus - Idiopathic - White matter tracts destroyed
Who is likely to suffer from Hydrocephalus
Biomodal
Young - Congenital malformations and brain tumours
Elderly - Strokes and tumour
What are the signs and symptoms of Hydrocephalus
Obstructive: Acute drop in conscious level - Low GCS
Diplopia - 6th Nerve palsy
Papilloedema
Neonates: Increased head circumference + Sunset sign (Downward conjugate deviation of the eyes)
Normal pressure: Triad: Dementia Gait disturbance Urinary incontinence Hyper-reflexia
What are the investigative signs of Hydrocephalus
Ventricular enlargement - CT
CSF from ventricular drainage may indicate pathology
LP contraindicated if raised ICP but therapeutic for normal pressure hydrocephalus
What are the causes of Transient ischaemic attacks
Usually embolic but may be thrombotic - Usually from a carotid atherosclerosis
Emboli can also arise from the heart due to AF, Mitral valve disease or Atrial myxoma
Clots from the right side can cause stroke if there is a septal defect
RFs: HTN, DM, HD, Hyperlipidaemia, Alcohol, Smoking, Peripheral artery disease, Polycythaemia ruby vera, COCP, Clotting disorders
What are the typical history of a Transient ischaemic attack
Brief duration of symptoms + Report of neurological defect
Unilateral symptoms Increased BP on presentation Focal neurological deficit on examination No positive symptoms No headache No epilepsy Hx Migraine Hx Cardiac disease
Carotid Bruit
What are the investigative findings in Transient ischaemic attacks
Potential Blood glucose - Hypo Coag - Coagulopathy ECG - AF MRI/CT Head- Half will have positive diffuse images Echo
How is Transient ischaemic attack treated?
Atherosclerotic / Small-vessel
1st - Antiplatelet = Aspirin, Clopidogrel
+ Antihypertensive
+ >50% Carotid stenosis - Endarterectomy or stent
Cardioembolic no IHD
1st - Anticoagulant = Warfarinf/Noax
2nd - Antiplatelet + Statin
Cardioembolic + IHD
1st - Anticoagulant + Statin
What are the 2 main types of seizure
Focal: Specific cortical regions (Complex/Simple)
Generalised: Affect the whole brain affecting consciousness
What are the 5 main types of generalised seizure
Tonic-Clonic Myotonic Absence Atonic Tonic
What are the causes of Epilepsy?
Most idiopathic Cerebrovascular disease Head injury Cranial surgery CNS infections Neurodegenerative Autoimmune diseases Tumour Drugs Metabolic: Uraemia, Hypoglycaemia, Hypo/Hypernatraemia, Hypo/Hypercalcaemia
What are the presentations of Epilepsy
Generalised seizures cause disturbance in consciousness. Tonic, Clonic, Postictal phases.
Seizures associated with tongue biting and incontinence.
In the postictal phase there is often headache and drowsiness. Amnesia both the event and circumstance
Absence - Interruption to mental activity for less than 30 seconds
Focal - Aura, focal motor activity during seizure, automatisms
What investigations are performed in Epilepsy
EEG - Confirm diagnosis, classify
CT/MRI - Shows structural, space-occupying or vascular lesions
How is Epilepsy treated
Focal - Carbamazepine or lamotrigine
Generalised - Sodium Valproate
Status epilepticus - Diazepam
+ Patient education
What are complications of Epilepsy
Fractures
Behavioural problems
Sudden death in epilepsy
Neutropenia + Osteopenia - Carbomazepine
What are the main causative organisms in Meningitis
Meningococcus or pneumococcus.
Less commonly Haemophilus influenzae; Listeria or TB if immunocompromised eg HIV +ve, organ transplant, malignancy
Viral: HSV, VZV, enteroviruses. CMV,
Fungal: Cryptococcus
What are risk factors for Meningitis
Crowded space Basal skull fractures Mastioditis Sinusitis Inner ear infections Alcoholism Immunodeficiency Splenectomy Sickle cell anaemia CSF shunts Intracranial surgery
What are the signs and symptoms of Meningitis
Early: Headache, Fever
Later: Photophobia Neck stiffness Irritability Drowsiness Vomiting Lowering GCS
Travel and exposure history!
Signs Kernig's sign Brudzinski's sign Skin rash - Non-blanching Hypotension Tachycardia Altered mental status
What are appropriate investigations in Meningitis
CSF:
Bacterial - Turbid, PMN, Low Glucose, Higher Protein
TB - Fibrin web, Lympho, Low Glucose, Highest Protein
Virus - Clear, Lympho, High Glucose, High Protein
How is Meningitis treated
IV Antibiotics - Ceftriaxone, Amoxicillin
Dex IV
Airway support
Fluid restriction
What are the possible complications associated with Meningitis
Septicaemia Shock DIC Renal failure Seizures Raised ICP
Outline the aetiology of Stroke
Ischaemic (80%): Thrombosis - Small vessel - Lacunar - Large vessel - Prothrombic state (Dehydration, thrombophilia)
Emboli
- Carotid dissection/athersclerosis, AF
Hypertension
- Watershed zones infarct when blood pressure is below auto regulatory range
Vasculitis/Cocaine
Haemorrhagic (20%):
- Hypertension
- Microaneurysm
- Amyloid antipathy
- Arteriovenous malformations
What are the different presentations of Stroke based on location
Anterior circulation: Anterior cerebral artery
- Contralateral Hemiparesis - Legs more than arms
- Confusion
- Executive function disturbances
Anterior circulation: Middle cerebral artery
- Facial weakness
- Contralateral Hemiparesis - Arms more than legs
- Contralateral Hemisensory loss
- Hemianopia
- Aphasia if left sided
Posterior Circulation: Posterior cerebral:
- Homonymous Hemianopia
- Visual agnosia
Anterior inferior cerebellar
- Vertigo, ipsilateral ataxia, ipsilateral deafness, ipsilateral facial weakness
Posterior inferior cerebellar
- Vertigo, ipsilateral ataxia, ipsilateral Horner’s syndrome, ipsilateral hemisensory loss, dysarthria, contralateral spinothalamic sensory loss
How is a stroke diagnosed
Non-contrast CT head within 25 mins - Excludes haemorrhage
MRI after if available
ECG - Check for arrhythmia
Echo - Cardiac thrombus
CT Angio - Detect dissections or intracranial stenosis
Carotid doppler - Check carotid artery disease
Bloods - Glucose, U&Es, Cardiac enzymes
How is stroke treated
<4.5 Hrs with no contraindications to thrombolysis:
1st Line - Alteplase 0.9mg/Kg (10% as bolus with remaining 90% as infusion over 1hr) Max 90mg
A - Aspirin 24hrs after Alteplase 300mg
+ Supportive (O2, Glucose, BP, Fever)
+ Swallowing assessment
A - Prophylactic VTE and early mobilisation (Heparin/LMWH)
> 4.5 Hrs with no contraindications to thrombolysis:
1st Line: Aspirin 300mg
+ Supportive
+ Swallowing assessment
A - Prophylactic VTE and early mobilisation (Heparin/LMWH)
Cerebral venous sinus thrombosis:
- Anticoagulation (Heparin/Warfarin)
+ Supportive
+ Swallowing assessment
Contraindications to thrombolysis include:
- Negative CT head
- Head trauma
- MI
- GI or UG Haemorrhage
- Recent surgery
- Hx IC Haemorrhage
What are complications of Stroke
Cerebral oedema Immobility Infections DVT Cardiovascular events Death
What are the different types of MS
Relapsing-remitting - Most common - Clinical attacks of demyelination with complete recovery
Clinically isolated syndrome - Single clinical attack of demyelination 10-50% progress to MS
Primary progressive MS - Steady accumulation of disability with no relapsing-remitting pattern
Marburg Variant - Severe variant of MS leading to advanced disability or death within weeks
