Neurology Flashcards
STROKE
What is it?
Ischaemic infarction or brain haemorrhage
STROKE
Risk factors?
- HTN
- DM
- HD
-PVD
Previous TIA
STROKE
Cause?
- Vessel occlusion
- Cardiac Emboli
CNS bleeds e.g. aneurysm rupture
STROKE
Number of deaths?
1 per 1000 per year
Clinical Presentation of ACA Stroke
1) Leg weakness
2) Sensory disturbances in leg
3) incontinence
4) Gait apraxia (can move lying down but cant walk)
5) drowsiness
Clinical Presentation of MCA Stroke
1) Contralateral arm+leg weakness
2) Contralateral sensory loss
3) hemianopia
4) Aphasia (language impairment)
5) Dysphagia
6) facial droop
Clinical Presentation of PCA Stroke
1) contralateral hemianopia
2) Cortical blindness
3) Visual agnosia (inability to process sensory information)
4) facial blindness
5) Facial droop
Clinical Presentation of Lateral Medullary Infarct occlusion of PICA (brainstem)
1) ipsilateral horner’s syndrome
2) Vomiting
3) Vertigo (environment or you are spinning)
4) Cerebellar signs
5) Facial numbness
What is Horner’s syndrome characterised by?
classic triad of miosis (ie, constricted pupil), partial ptosis, and loss of hemifacial sweating (ie, anhidrosis).
Miosis
Ptosis
Anhidrosis
STROKE
tests?
ACT FAST
- CT/MRI
- ECG for MI/AF
- CXR FOR LVH
STROKE
Posterior circulating stroke features?
- Vomit/vertigo/nausea
- Dysarthria/ speech impairment
- motor deficit
- locked in
- visual disturbances
STROKE
Acute treatment? within 1 hour
- protect airway
- check pulse, BP, ECG
STROKE
Within 4.5 hours?
thrombolysis (IV alteplase)
STROKE
how should a patient by hydrated?
IV so no choking.
food assistance and TED stockinga
STROKE
Primary prevention?
- Reduce Risk Factors
statins, smoking, DM, HTN, exercise
STROKE
Secondary prevention
- Antiplatelet (clopidogrel)
+ Aspirin
+ AF/BP treatment - Warfarin if cause was AF
TRANSIENT ISCHAEMIC ATTACK (TIA)
Cause?
1) microemboli- which then lyse, from atheromas or thrombus
2) Temporary decrease in cerebral perfusion
TRANSIENT ISCHAEMIC ATTACK (TIA)
Risk Factors?
- HTN
- DM
- Smoking
- Hyperlipidaemia
- Obesity
- High alcohol
TRANSIENT ISCHAEMIC ATTACK (TIA)
What is the definition?
- Sudden onset focal neurological deficit with symptoms that are maximal at onset and usually resolve within 15 minutes
TRANSIENT ISCHAEMIC ATTACK (TIA)
carotid Symptoms?
- Amaurosis Fugax (emboli in retinal artery)
- Aphasia (language impairment)
- Hemiparesis (one side weakness)
- Hemisensory loss
- Hemianopia visual loss
TRANSIENT ISCHAEMIC ATTACK (TIA)
Vertebrobasilar symptoms?
- Diplopia (double vision)
- Vertigo/ vomit
- Ataxia (lack of voluntary coordination of muscle movements)
- tetraplegia
- Hemisensory loss
- choking and dysarthria (hard to speak)
- hemianopia visual loss
What is Amaurosis Fugax?
- progressive visual loss in one eye. ‘curtain descending’
TRANSIENT ISCHAEMIC ATTACK (TIA)
Investigation?
- FBC, ESR, Glucose, lipids, U+E
CXR
ECG
What is a ABCD2 score?
Determines time frame needed to investigate a stroke (score of 6+ means 35.5% of stroke in next week)
list the different reasons to get a point for the ABCD2 score?
- Age >60 = 1 point
- BP >140/90 = 1 point
- Unilateral weakness = 2 points
- speech problems + weakness = 1 point
- Duration >1 hour = 2 points <1 hour = 1 point
- diabetes = 1 point
What investigations need to be done for a high/low ABCD2 score?
high = MRI & carotid doppler ultrasound within 24 hours
low = same but within a week
treatment of TIA?
- control CVS risks
- Aspirin + Clopidogrel
- Carotid Endarterectomy if necessary within 2 weeks
SUBARACHNOID HAEMORRHAGE
What is it?
spontaneous bleeding in sub-arachnoid space and they account for 5% of all strokes
SUBARACHNOID HAEMORRHAGE
most common causes?
- berry aneurysm rupture 70%
- arterio-venous malformations 15%
- idiopathic 15%
Common sites for berry aneurysms?
1) bifurcation of middle cerebral
2) Junction of posterior and internal carotid
3) Junction of anterior communicating and anterior cerebral
SUBARACHNOID HAEMORRHAGE
Symptoms?
- sudden onset of worst headache ‘ever’
- Vomit / nausea
- loss of conciousness
SUBARACHNOID HAEMORRHAGE
Signs
- Kernig’s (inability to straighten knee when hip flexed 90 degrees)
- Brudzinski’s- neck stiffness - flex neck and knee+hip flex too
SUBARACHNOID HAEMORRHAGE
Investigations?
CT (Blood in sulci)
if negative do LP 12hrs after
blood becomes yellow due to bilirubin and oxyhaemoglobin degradation ( Xanthochromia)
SUBARACHNOID HAEMORRHAGE
Treatment?
- bed rest + supportive care
- CCB’s and control of HTN
surgeon may be able to coil/ clip aneurysm
What is a subdural haemorrhage?
Bleeding from bridging veins between cortex and sinuses (below dura)
What is an extra-dural haemorrhage?
tear in dural venous sinus due to fractured temporal/parietal bone
How long do sub/extra dural haemorrhages take to develop? why do they take this long?
can take a very long time
1) pressure change is small
2) clot degrades
3) increased osmotic pressure - enlarges due to H20
investigation and treatment of sub/extra dural haemorrhages?
clot evacuation
CT shows haematoma
treatment - Surgery
INTRACEREBRAL STROKE
Types? and what is the percentage of intracerebral out of all strokes?
Hypertensive
Lobar
15% of all strokes
INTRACEREBRAL STROKE
Clinical features?
1) Loss o consciousness
2) Stroke features
3) severe headache
Cause of hypertensive bleed?
Charcot-Bouchard aneurysm due to longstanding HTN
Leaking due to microbleeds across the brain = bad prognosis
What are Lobar bleeds associated with?
dementia (B-amyloid deposition in vessel walls)
Features and location of hypertensive bleedas?
deep and small bleeds in the basal ganglia, pons and cerebellum
INTRACEREBRAL STROKE
Investigations?
ABC and CT of head
what is Hydrocephalus?
blood in ventricles and clots them off
small vessels become blocked so more ischaemia = immediate neurosurgery
INTRACEREBRAL STROKE
Treatment?
BP control
labetolol + GTN spray immediately
EPILEPSY
Different types of seizures?
generalised Tonic-Clonic Seizure Absence Seizure Myotonic/clonic Akinetic/Atonic Motor seizure temporal Frontal occipital parietal
Describe a generalised tonic-clonic seizure
1) Period of ridgity (tonic) followed by rhythmical jerks (clonic)
2) Then drowsy/coma for a few minutes
describe an absence seizure
Cessation of activity and staring for a few seconds
describe a Clonic seizure
Isolated muscle jerking
Describe a Tonic Seizure
Stiffness of body
Describe an Atonic Seizure
loss of moving = falling and loss of consciousness
What happens if a partial seizure becomes a generalised seizure?
still classes as partial
describe a motor seizure
Motor cortex - jerky movements to contralateral limbs of seizure
may be paralysis few hours later
What is the post-ictal state
After seizure headache, confusion, myalgia, weakness
Temporal Seizure effects?
visual/olfactory hallucinations.
Deja vu
Jemais vu - things feel unfamiliar
Frontal seizure effects?
speech/motor movement loss
EPILEPSY
Cause?
unknown
flashing lights possibly
EPILEPSY
Signs of EPILEPTIC?
- tongue bite
- cyanosis
- incontinence
- head turn
- less than 5 min
- drowsy and muscle pain
EPILEPSY
Signs of Syncope?
- Upright position, sweating and vomit before/after
EPILEPSY
Signs of NON-EPILEPTIC?
- eyes closed
- talking
- crying
- long duration
EPILEPSY
Investigations?
MRI and video EEG
EPILEPSY
Treatment of generalised TOnic-clonic?
Sodium Valproate or Lamitrigine
EPILEPSY
Treatment of PArtial?
Carbomazepine
EPILEPSY
Treatment of Absence?
same as GTC + ethosuximide
Sodium valproate or Lamitrigine + ethosuximide
EPILEPSY
treatment of tonic/ Myotonic/ Atonic
sodium valproate or Lamitrigine (avoid carbamazepine)
treatment of severe EPILEPSY?
surgery 1) lobe removal/ removal of problematic area
2) Vagal Nerve stimulation
How does carbamezapine work?
1) Blocks Na+ channels = decreased firing of neurones and glutamate
Side effects of Carbamezapine?
Nausea vomiting drowsy double vision dizziness
how does valproate work?
1) Blocks transmembrane Na+ -stabilises neuronal membranes
Side effects of valproate?
hepatotoxicity
hair loss
increased appetite
When should you avoid using Valproate?
pregnant and hepatic disease patients
DEMENTIA
What is the percentage change of someone to get dementia at the following ages :
> 65
80
100
5-10% >65
20%>80
70%>100
DEMENTIA
Aetiology?
- Alzheimer’s (65%)
- vascular (25%)
- lewy bodies (15-25%)
DEMENTIA
What is inevitable for someone with Down’s Syndrome?
Alzheimer’s disease
DEMENTIA
Clinical Features of Alzheimer’s?
1) Decrease in neurone number
2) neurofibrillary tangles
3) accumulation of B-amyloid plaques
DEMENTIA
Symptoms of Alzheimer’s?
INITAL = Memory loss over months/years
progressions
1) All aspects of cerebral function
2) Decrease in language
3) Intellect, verbal and memory loss
4) Agnosia (cant recognise things)
5) Visuospacial skills lost
DEMENTIA
General non cognitive symptoms?
- Aggression
- Depression
- Hallucinations
- Agitation
- Apathy
DEMENTIA
tests?
MMSE
CT for young patient
Good history/ timeline required
bloods- FBC, thyroid, LFTs, B12/folate (exclude other causes)
DEMENTIA
treatment?
- Donepazil
- Rivastigmine
- SSRI’s (depression)
When is Vascular Dementia common and how is it characterised?
Common after strokes
characterised by periods of stability then sharp decline
what is Lewy Body Dementia?
- fluctuating cognition with variation of attention
Clinical features of Lewy Body Dementia?
- Hallucinations
2) Parkinson’s
3) Sleep problems
4) Depression - may not have memory loss early on!
MULTIPLE SCLEROSIS
Types?
- relapsing-remitting
- primary Progressive (no Rx)
- Secondary progressive
MULTIPLE SCLEROSIS
Epidemiology?
1/1000 F:M 3:1
MULTIPLE SCLEROSIS
Risk factors?
- Epstein-barr Virus
- urban western living
- low vitamin D
- Female
- Genetics
MULTIPLE SCLEROSIS
pathology?
1) Antigens against CNS made due to exposure to a similar antigen (e.g. EBV)
2) T-lymphocytes cause problems when they cause the blood-brain barrier
MULTIPLE SCLEROSIS
Cause?
- Demyelination of oligodendrocytes and axonal damage
- Myelin recovers whereas the axons don’t
- Shorter gaps between the Nodes of Ranvier due to thin myelin = slow conduction
MULTIPLE SCLEROSIS
Where is inflammation likely to be found?
Brain = Ventricles
Spinal Cord = Posterior column
MULTIPLE SCLEROSIS
clinical Features?
1) Optic neuritis
2) Pain
3) Spasticity
4) paraesthesia (pins and needles)
5) Bladder/sexual dysfunction
6) Nystagmus (involuntary eye movement)
7) vertigo
8) Diplopia (double vision)
MULTIPLE SCLEROSIS
Exacerbating factors?
- STRESS
- HOT TEMP
MULTIPLE SCLEROSIS
diagnosis?
- > 2 CNS symptoms disseminated in time and space
- MRI shows plaques/inflammatory lesions around ventricles
IgG monoclonal bands
MULTIPLE SCLEROSIS
Treatment of Acute relapse?
Steroids
Vit D and stress free
MULTIPLE SCLEROSIS
Treatment?
1) Interferon beta (prevents immune activation)
2) glatiramer acetate (similar to myelin)
3) Natalizumab prevents t-lymphocytes crossing blood-brain barrier
MULTIPLE SCLEROSIS
Lifestyle adaptations?
- vit D supplements and stress free
MULTIPLE SCLEROSIS
medicine for Spasticity?
baclofen
MULTIPLE SCLEROSIS
medicine for Tremors?
Beta blockers
MULTIPLE SCLEROSIS
Medicine for incontinence
Tolterodine
Oxybutynin
PARKINSON’S
Pathology?
- Mitochondrial DNA dysfunction causes degeneration of dopaminergic neurones In the substantia nigra pars compacta
- Synuclein deposition leads to Lewy bodies and decreased dopamine
PARKINSON’S
Aetiology?
Mitochondrial DNA dysfunction and oxidation stress
Idiopathic
PARKINSON’S
Risk Factor genes?
SNCA and PRKN genes
PARKINSON’S
Cardinal Triad?
1) Tremor
2) Ridgity
3) Bradykinesia
PARKINSON’S
Describe the Tremor
- worse at rest
- ‘pill rolling’ of thumb over fingers
- asymmetrical and gradual
PARKINSON’S
Describe the Ridgity
- Cogwheel ridgity
- Whole ROM is rigid
- Felt especially through rapid pronation/supination
PARKINSON’S
Describe Bradykinesia>
- slow initiation of movements
- Shuffle steps
- Decreased arm swing
- Freezing at obstacles
- Slow blinking
PARKINSON’S
Postural Effects?
- Shuffle
- Stoop
- Decreased arm swing
- poor balance
PARKINSON’S
Non motor effects?
- Depression
- constipation
- Micrographia (abnormally small, cramped handwriting)
- Dementia
PARKINSON’S
tests?
Ct to exclude other causes
PARKINSON’S
treatment?
1) Postural Exercises
2) L-Dopa and Carbidopa
3) Dopamine Agonists
4) MAO-B Inhibitors
5) COMT inhibitors
Give an example of a Dopamine Agonist
Ropinirole
Give an example of a MAO-B inhibitor
Rasagiline
Give an example of a COMT inhibitor
Entacapone
What is the function of COMT and MAO-B enzymes?
convert Dopamine into DOPAC + HVA.
To treat Parkinson’s we need as much dopamine as possible therefore these enzymes need to be inhibited
BRAIN TUMOURS
Name some different types and their percentage of occurrence
Primary Malignant (35%)
Benign (15%)
Metastases (50%)
BRAIN TUMOURS
Of Primary malignant BT’s, how many are Astrocytomas and how many are oligodendrogliomas?
Astrocytomas (90%)
oligodendrogliomas (5%)
BRAIN TUMOURS
a brain tumour will cause an increased intra-cranial pressure, what effects would this pressure increase have
Headache + confusion
headache worsens: 1) Morning 2) leaning forward
3) cough/straining
BRAIN TUMOURS
Pathology of an increased ICP
1) brain displaced downwards
2) Pressure on brainstem
3) drowsiness and respiratory depression
BRAIN TUMOURS
Clinical presentation? (apart from raised ICP)
- neurological deficit (depending where the tumour is)
- focal epilepsy (need a CT to exclude a tumour if someone has a new seizure)
BRAIN TUMOURS
Tests?
CT/MRI and PET scan
BRAIN TUMOURS
Treat?
Surgery/radiotherapy
BRAIN TUMOURS
what is given for rapid relief of symptoms?
IV Dexamethasone
What does Dexamethasone do?
reduce cerebral oedema
Where the most common sites of Mets to the brain?
- lung
- breast
- colon
- skin
- kidney
BRAIN TUMOURS
Any associated mutations?
50% of tumours have methylated MGMT mutation
BRAIN TUMOURS
What does having a methylated MGMT mutation mean?
Sensitive to Temozolomide so a better prognosis
BRAIN TUMOURS
What may mean a good prognosis for someone with a brain tumour?
- under 50
IDH mutation
MGMT mutation
What may mean a bad prognosis for someone with a brain tumour?
- over 50
- no IDH or MGMT mutation
What is Kernig’s and brudzinski’s signs?
- Kernig’s (inability to straighten knee when hip flexed 90 degrees)
- Brudzinski’s- neck stiffness - flex neck and knee+hip flex too
MENINGITIS
cause?
Meningococcus or Pneumococcus
immunocompromised = Cryptococcus
Unvaccinated = H.influenzae
Elderly = S.pneumoniae
MENINGITIS
Early Clinical Features?
1) Headache
2) Fever
3) kernig’s sign
4) brudzinksi’s sign
MENINGITIS
later Clinical Features?
- Decreased consciousness
- Stiff neck
- Photophobia
- Non-blanching petechial rash
- Seizures
MENINGITIS
Investigations?
1) Blood cultures
2) Lumbar Puncture
3) IV cefotaxime
4) Head CT
5) Bacterial + viral throat swabs
6) PCR for meningococcus and Pneumococcus
MENINGITIS
When should you not do a lumbar puncture
When there is a risk of cerebral coning
MENINGITIS
When should a CT be done first?
If raised ICP
MENINGITIS
How would bacterial lumbar puncture look?
- cloudy
- high neutrophils
- low CSF
- high protein
MENINGITIS
How would a viral Lumbar Puncture look?
- Clear
- high lymphocytes
- normal CSF
- Normal to high protein
MENINGITIS
Which is more serious bacterial or viral?
bacterial, there is also no rash with viral
MENINGITIS
treat?
IMMEDIATELY = IV Cefotaxime and ampicillin
also IV Dexamethasone
ENCEPHALITIS
What is it?
Inflammation of brain parenchyma
ENCEPHALITIS
Clinical features?
- Altered mental state
- motor and sensory deficits
1) fever
2) headache
3) loss of consciousness
4) lethargy PROGRESSES into seizures
ENCEPHALITIS
Cause?
Usually virally by Herpes Simplex Virus
immunocompromised are at risk
ENCEPHALITIS
investigation|?
1st- CT
2nd- LP for viral findings
ENCEPHALITIS
Treatment?
IV acyclovir IMMEDIATELY
What is Shingles?
reactivation of dormant Herpes zoster virus in dorsal root ganglion
Features of Shingles?
dermatome distribution of pain and a rash (papules and vesicles)
Treatment of shingles?
PO Acyclovir
Headache red flags?
1) papilloedema (optic disc swelling that is caused by increased intracranial pressure)
2) seizure
3) Cancer history
Urgent referrals for headache?
- suspected Meningitis
- thunderclap headache
- Red eye (glaucoma)
What is Aura?
Patient knows about a seizure e.g. strange feeling in gut
Migraine Diagnostic Criteria without Aura?
1) >5 attacks
2) they last 4-72 hours
3) Nausea/Vomiting
4) unilateral/Pulsating
5) aggravated by movement
20% of migraines have aura, what may this be?
1) Flashing lights (visual)
2) tingling (sensory)
3) Dysphagia (speech)
Partial triggers of headaches? (50%)
Chocolate Hangovers Orgasm Cheese Oral contraceptives Lie ins Alcohol Tumult (loud noise) Exercise
abortive treatment of headaches?
NSAIDs/paracetamol
+ PO rizatriptan (migraines)
Preventative treatment for migraines?
1st- propranolol or amitriptyline or topiramate
2nd- valproate/Botulinum toxin type A
How do migraines happen?
1) changes in brainstem blood flow = unstable trigeminal nuclei
2) Inflammatory mediators released
3) These impact on trigeminal nerve nucleus
MOTOR NEURONE DISEASE
characteristics?
- Relentless and unexplained destruction of:
- UMN
- anterior horn cells
cranial nerve nuclei
MOTOR NEURONE DISEASE
what does it never affect?
- Sensory
- Ocular movement (eye)
- sphincters
MOTOR NEURONE DISEASE
What will most people die of if they have MND within 3 years?
Respiratory failure - bulbar palsy / pneumonia
MOTOR NEURONE DISEASE
Cause?
oxidative stress and free radicals
What is Oxidative stress
Oxidative stress is essentially an imbalance between the production of free radicals and the ability of the body to counteract or detoxify their harmful effects through neutralization by antioxidants
MOTOR NEURONE DISEASE
Clinical features of Amyotrophic lateral Sclerosis (50%)
- Lateral corticospinal tracts and anterior horn cells affected;
1) Progressive spastic tetraplegia
2) Split hand sign; thumb side of hand appears separated due to excessive wasting (thenar muscles disproportionately wasted as compared to the hypothenar muscles)
MOTOR NEURONE DISEASE
what does Progressive muscle Atrophy affect (10%)
- LMN lesion
- distal 1st to be affected
- NO UMN signs
MOTOR NEURONE DISEASE
what does Progressive Bulbar Palsy affect (10%)
Cn 9-12 affected
LMN lesion of:
tongue (fasciculations)
speech - dysarthria
swallowing dysphagia
MOTOR NEURONE DISEASE
give examples of UMN signs?
- Spasticity
- brisk reflexes
- Upgoing plantars (Babinski reflex)
SEE TABLE IN NOTES
What is the Babinski reflex?
when the sole of the foot is stimulated with a blunt instrument. The reflex can take one of two forms. In normal adults, the plantar reflex causes a downward response of the hallux. An upward response of the hallux is known as the Babinski response
MOTOR NEURONE DISEASE
LMN signs?
- Wasting
- tongue fasciculations
- abdo,back,thigh fasciculations
SEE TABLE IN NOTES
MOTOR NEURONE DISEASE
Investigations?
1) EMG - shows muscle degeneration (electromyography)
2) MRI + LP (exclude inflammatory types)
MOTOR NEURONE DISEASE
treatment?
Drug dysphagia Resp failure Drooling spasticity
1) Riluzole (blocks Na+ channels = less glutamate) PEG feeding - Dysphagia ventilatory support -resp failure amitriptyline - Drooling Baclofen - spasticity
MYASTHENIA GRAVIS
Epidemiology?
40-60s, mainly women
MYASTHENIA GRAVIS
Pathology>
- Autoimmune disease mediated by A-bodies to nicotinic ACh receptors
- both T/B cells involved
- Depletion of Post-synaptic receptors
MYASTHENIA GRAVIS
Associations?
50 years - Thymic hyperplasia / atrophic / tumour
MYASTHENIA GRAVIS
Clinical Features?
Fatigability of muscle on sustained activity that gets better with rest
Ocular muscles affected 1st then moves down
speech
chewing
swallowing
breathing
MYASTHENIA GRAVIS
Specific features?
- ptosis (eye-lid droop)
- diplopia (double - vision)
- Voice fade
MYASTHENIA GRAVIS
Diagnostic test?
ask patient to hold up arms and they will fall
MYASTHENIA GRAVIS
Scientific investigations?
- Autoantibodies to AChR in 90% of cases
- Autoantibodies to MuSK
- CT of thymus
- See if ptosis improves by 2mm when ice applied for >2 mins
MYASTHENIA GRAVIS
treatment?
1st - symptom control - Pyridostigmine (anticholinesterase)
2nd - Steroids (prednisolone)
3rd- thymectomy
TENSION HEADACHES
Cause?
Depression and anxiety
TENSION HEADACHES
Diagnostic Criteria?
1) >10
2) Last 30 mins - 7 days
3) 2 of: bilateral pain, pressing/tightening
4) mild/moderate
5) Not triggered by exercise
TENSION HEADACHES
treat?
paracetamol/NSAIDs - not overusing analgesia
CLUSTER HEADACHES
Diagnostic Criteria
1) >5
2) Severe
3) unilateral
4) temporal/orbital pain
5) 15-180 mins
6) Restlessness and agitation
7) Occurs every other day, as many as 8 each day
CLUSTER HEADACHES
Acute Treatment?
100%O2 for 15 mins
Subcutaneous Sumatriptan
TRIGEMINAL NEURALGIA
What is it?
Compression on trigeminal root e.g. aneurysm or tumour
TRIGEMINAL NEURALGIA
Diagnostic criteria
- Severe, stabbing pain lasting seconds-mins
- Precipitated by stimuli to the face
TRIGEMINAL NEURALGIA
Treat?
carbamazepine
CAUDA EQUINA SYNDROME
Where does the spinal cord end
L1/L2
CAUDA EQUINA SYNDROME
cause?
Lumbar disc prolapse - L4-L5 and L5-S1
CAUDA EQUINA SYNDROME
associated with?
bladder and bowel dysfunction
and perianal numbness (saddle paraesthesia)
CAUDA EQUINA SYNDROME
Signs?
1) back pain
2) leg weakness
3) Numbness
4) decreased reflexes
CAUDA EQUINA SYNDROME
treat?
MRI of spine and surgical decompression
NEUROPATHIES
Cause?
acute compression and entrapment
NEUROPATHIES
Common mononeuropathies?
median
ulnar
common peroneal
radial- (wrist drop)
POLYNEUROPATHIES
Sensory Symptoms?
- Pins and needles
- Numbness
- Pain in extremities
- Tingling
‘glove and stocking’ - numbness in distal areas (hands and feet)
POLYNEUROPATHIES
Motor symptoms?
weakness
POLYNEUROPATHIES
Autonomic Symptoms?
- Postural Hypotension
- erectile dysfunction
- Sweating
- diarrhoea
POLYNEUROPATHIES
Causes?
Diabetes Alcohol Vit B12 deficiency Infections (Guillain-Barre) Drugs (isoniazid)
POLYNEUROPATHIES
treatment?
- weak opiates
- SSRI’s/TCAs
- treat cause
- Physiotherapy
CARE OF UNCONCIOUS PATIENT
What are the severity ranges on the Glasgow coma score?
mild >13
moderate 9-12
severe <8
CARE OF UNCONCIOUS PATIENT
What cant they do?
1) gag
2) Circulating depression
3) cant maintain airway
4) No protection
CARE OF UNCONCIOUS PATIENT
1st line treatment?
basic life support
CARE OF UNCONCIOUS PATIENT
Acute life support is made up of?
1) Intubation
2) IV fluids
3) Drugs to maintain circulation
4) venous access
CARE OF UNCONCIOUS PATIENT
Intensive care?
same as acute ,life support +:
- catheter
- tracheal suction
- nutrition
- pressure sore prevention
GIANT CELL ARTERITIS
who is it common in?
elderly
GIANT CELL ARTERITIS
Symptoms?
1) Scalp tenderness
2) headache
3) Amaurosis Fugax (blind in 1 eye)
GIANT CELL ARTERITIS
Extracranial symptoms?
1) Dyspnoea
2) Morning stiffness
3) Unequal weak pulses
GIANT CELL ARTERITIS
Investigations?
RAISED- ESR, CRP, platelets, Alkaline phosphate
- low Hb
- temporal Artery Biopsy
GIANT CELL ARTERITIS
treatment?
immediate prednisolone
delay the risk of irreversible bilateral vision loss
HUNTINGTON’S
Features of Huntington’s?
- Chorea (involuntary movements)
- personality change
- ## Dementia
HUNTINGTON’S
what is it and what are its genetic components
-Incurable neurodegenerative disorder
- Autosomal dominant
- expansion of CAG repeat on chromosome 4 that produces mutant Huntington protein
HUNTINGTON’S
How does someone die of Huntington’s?
loss of basal ganglia neurones/ GABA/ ACh until death
SPINAL CORD COMPRESSION
Aetiology?
- Secondary malignancy in spine from (breast, kidney, lung, prostate, thyroid)
BKLPT
SPINAL CORD COMPRESSION
features?
weak legs
sensory loss
spinal pain
arm weakness often less severe
SPINAL CORD COMPRESSION
Signs?
Look for motor sensory and reflexes
1) normal above the lesion
2) LMN signs at the level of the lesion
3) UMN signs below the level of the lesion
SPINAL CORD COMPRESSION
Investigations?
Instant MRI
screening bloods and biopsy
CXR to check for lung malignancy
SPINAL CORD COMPRESSION
Treatment?
Malignant = IV Dexamethasone while waiting for Chemo/Radio
GUILLAIN-BARRE SYNDROME
What is it?
Acute inflammatory demyelinating polyneuropathy
GUILLAIN-BARRE SYNDROME
key clinical feature?
Progressive symmetrical ascending weakness (starting at the feet and moving up the body)
Reduced reflexes
There may be peripheral loss of sensation or neuropathic pain
It may progress to the cranial nerves and cause facial nerve weakness
GUILLAIN-BARRE SYNDROME
Cause?
Infective triggers (commonly post campylobacter gastroenteritis or EBV/CMV) cause antibodies to attack nerves
GUILLAIN-BARRE SYNDROME
How may death occur?
autonomic neuropathy = cardiac arrest
GUILLAIN-BARRE SYNDROME
Investigation?
1) lumbar puncture
- rise in protein with a normal white blood cell count (albuminocytologic dissociation) - found in 66%
2) nerve conduction studies may be performed
- decreased motor nerve conduction velocity (due to demyelination)
- prolonged distal motor latency
- increased F wave latency
GUILLAIN-BARRE SYNDROME
treatment?
IV immunoglobulins for 5 days and plasma exchange
What is Hydrocephalus?
abnormal build up of CSF (cerebrospinal fluid) in the cavities (ventricles) of the brain. The build-up is often caused by an obstruction that prevents proper fluid drainage
What does interferon beta do?
prevents immune activation1) Interferon beta (prevents immune activation
What is glatiramer acetate similar to?
Myelin
what does Natalizumab do?
prevent t-lymphocytes crossing the blood-brain barrier
classic triad of Meningitis?
- Photosensitivity
- Stiff neck
- Headache
