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Neurology > Pathology > Flashcards

Pathology Flashcards

1
Q

What is Brown-Sequard Syndrome?

A

Spinal Cord lesion affecting LMN
= Ipsilateral UMN paralysis loss of proprioception (touch + sensation)
Contralateral loss of pain and temperature, no reflex ( as pain crosses at entry deficit is on other side)

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2
Q

What happens to reflexes and muscle tone in an UMN lesion?

A

Paralysis (disrupted neurone pathway

But LMN pathway fine so exaggerated reflexes + tone= hyperreflexia, spastiparalysis

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3
Q

What is Electrophysiology used to diagnose?

A

Ulnar Neuropathy- cell sensory body in DRG alive but anterior horns + regions to spinal chord die.
Left with sensory + motor response from ulnar nerve but no action

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4
Q

What is Electromyography (EMG) used to diagnose?

A

NMD (tight relationship between fibres in motor units lost)= Jiter
eg./ Myathesthenia Gravis (autoimmune) antibodies to post synaptic ACh receptor = weakness and fatigue of facial muscles (+ ptosis + diplopia) treat via acetylcholinesterase inhibitor + immunosuppression

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5
Q

What is Electroencephalogram used to diagnose?

A

Looks at electrical activity within the brain
eg./ Ambulatory sleep study (over day + night)
Video telemetery- epilepsy
Encephalopathy, altered consciousness states

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6
Q

What happens to sensation if you damage the dorsal column?

A

Loose noxious mechanoreceptors on ipsiliateral side (hasn’t crossed yet)

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7
Q

What happens to sensation if get a lesion on anterolateral spinothalamic tract?

A

loose thermorecptive + nociceptive on contralateral side (cross immediately)

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8
Q

What is Right-Left Agnosia?

A

Lesion-Hemisensory neglect- can perceive sensations but can’t comprehend other side of the body

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9
Q

What is Acalculia?

A

Dominant lobe lesion- can’t count, write etc

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10
Q

What is Agraphia?

A

Less dominant lobe lesion- artistic + musical affects

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11
Q

What is Aphasia? What are the 2 different subtypes?

A

Problem with speech due to 1+ damaged areas in the brain

  1. Brocas Aphasia- Frontal lobe damage- understand + aware but miss small words + weakness/ paralysis of one side (motor cortex here)
  2. Wernicks Aphasia- Temporal Lobe Damage- fluent but meaningless speech, not aware NO paralysis
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12
Q

What are the 3 types of fibres found in white matter? What areas do they connect?

A
  1. Commisural Fibres- One hemisphere to another eg./ corpus callous
  2. Associated Fibres- Different lobes in 1 hemisphere (long/ short)
  3. Projection Fibres- Up (sensory) + Down (motor) through internal capsule (fibres passing to and from the cerebral cortex)
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13
Q

What is the basal ganglia? What is it made up of? What is its function?

A

A collection of neuronal cell bodies deep in cerebral hemispheres.
Composed of-
1. Caudate Nucelus
2. Lentiform Nucleus (putamen + globus pallidus)
3. Substantia Nigra (midbrain)
Regulates initiation and termination of movement (inertia)
Extrapyramidal- control of motor system

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14
Q

What kind of pathology is found in the basal ganglia?

A

Parkinsons
Chorea
Athetosis

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15
Q

What is hydrocephalus?

A

Excessive cerebrospinal fluid volume in IV spaces= dilation of ventricles + a wide range of symtoms

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16
Q

What is communicating hydrocephalus?

A

Non-obstructive
CSF production > CSF absorption OR CSF>
Uniform dilation= Inc ICP
Cause- Infection eg./ bacterial meningitis,
Subarachnoid haemorrhage, post op eg./ tumour gunge blocks, head trauma, choroid plexus papilloma (rare)

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17
Q

A neurological condition presents with-
Increased head circumference in neonates
and papillodema- diplopia/blurred vision, gout disturbance, 6th CN palsy, neck pain + upwards gaze difficulty in the rest of the population.
What is this pathology? How would you go about investigating and treating it?

A

Communicating (non-obstructive) hydrocephalus
6th nerve as passes through subarachnoid space
neck pain- tonsillar herniation
Investigate via Ct (asses ventricular size- will be dilated, 3rd ventricle ballooned), MRI, Ultrasonography in infants.
Treat via external ventricular drain (3 way tap into left ventricle (high infection risk) + mannitol (osmotic diuretic)/ communicating shunt

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18
Q

What in non- communicating hydrocephalus?

A

Obstruction
eg./ Aqueductal stenosis (kids, foramen of munro); tumours cancers and masses; cysts/ infection; haemorrhage/ haemotoma; Interventricular bleed, Spina Bifida Cystica.
Headaches in the morning are common
Treat via shunt, remove lesion (eg./ pineal tumour, ependyma, colloid cyst), 3rd ventriculostomy- hole in 3rd ventricle fluid bypasses cerebral aqueduct

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19
Q

What is normal pressure hydrocephalus?

A

Communicating Hydrocephalus on MRI. Normal opening pressure dementia like syndrome reversible with treatment via VP shunt (pressure is normal so hard to know how much to remove)
Hakims Triad- Wet, wobbly (gait) + wacky (dementia)

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20
Q

What clinical suspicion of disease would a lumbar puncture be required for? What are contraindications for carrying it out?

A 
To Investigate- Meningitis
Subarachnoid Haemorrhage (bilirubin levels)
Meningioencephalitis (WBC)
Malignancy (cytology)
Infusion of drugs/ contrast
Contraindications-
Cardiac/ respiratory instability
Localised skin/ soft tissue infection
Inc ICP (head CT first)
Chiari Malformation (tonsillar herniation)
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21
Q

how is a lumbar puncture carried out?

A
  1. Povidone- Iodine + wand + fenestrations
  2. Anasthetic eg./ lidocaine
  3. Spinal needle thorugh L3-4/4-5
  4. manometer, stopcock + tubing
    Through erector spinal + ligament flavulum + dura (double pop)
    Collect 3 tubes (Culture + gram, glucose + protein, cell count/ differential)
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22
Q

What are the complications of a lumbar puncture?

A

Spinal headache/ blackout
Epidermal occlusion cyst
Herniation- intubate, IV saline, bed back to 30-40
Nerve Trauma- feels like electric shock to Pt, withdraw needle and try again, if long shock give corticosteroids and do nerve conduction studies

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23
Q

What can cause bilateral hippocampal damage and what affect can this have?

A

Herpes Simplex
Long term memory before the damage will be intact + immediate sensory + reflective intact (as they don’t require retention through papez circuit) BUT loose ability to form new long term memories

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24
Q

How is amnesia caused? What are the 2 subdivisions?

A

Caused by disruption of reverberating neuronal circuit eg./ by head injury/ infection
1. Anterograde Amnesia- Inability to recall events AFTER incident (shot lived/ permanent)
2. Reterograde Amnesia- Can’t remember events BEFORE injury (can recall old)
Usually both present together.
If thalamus damaged but hippocampus intact get retrograde only (thalamus needed to search existing memory bank)

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25
Q

What is Korsakoffs Syndrome?

A

Chronic Alcoholism (dec in Vitb1)- damages limbic system (reduced ability to consolidate memories)

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26
Q

What is Alzthehiemers?

A

Severe loss of cholinergic neurones (including in hippocampus)= memory loss (anti-cholinesterase improve but still underlying degeneration)

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27
Q

A viral infection can cause damage to sensory inputs (proprioception) at spinal level. What would happen as a result of this?

A

Neurones in DRG die (don’t regenerate) loss of body in space- rely on visual system to provide feedback

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28
Q

What are the clinical signs of an UMN lesion? Why do these occur?

A

Normally synapse with LMN to regulate ⍺motor-neurone activity
lesions- spasticity (continuous contraction causes stiffness/ tightness), paralysis, transient, brisk reflexes, Babinski sign

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29
Q

What is the motor functionality difference between the corticospinal tract vs rubrospinal tract vs reticulospinal tract? How will this affect a clinical signs of a lesion?

A

Corticospinal is lateral- descending control of ‘skilled’ motor to extremities so will get paresis (weakness) NOT paralysis with lesion here.
Rubrospinal is anterior to cortispinal- descending facilitate flexors + inhibit extensors (balance control) fine tuning and fraction (1 joint only movement) affected.
Reticulspinal is anterior- descending cortical control of voluntary motor function

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30
Q

What is spinal shock?

A

Damage to spine- firing at abnormal rates= trauma to spinal chord (loss of brain-muscle connections)
Loose sensation, bowel, bladder + sexual regualation (autonomic)
Reflexes return but exaggerated + clonus. Loose excitation above lesion but works below

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31
Q

How does a LMN lesion present?

A

Nerve and neuronal cell body destroyed- paralysis + NO reflexes
Arflexia, Flaccid paralysis

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32
Q

How do epileptic seizures occur?

A

Abnormal firing of high frequency APs creates a wave across the cortex-marches- fingers- arms- face etc

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33
Q

How does UMN Syndrome occur?

A
  1. Cortical Damage= hypotonia (spinal shock), Babinski sign
  2. Removal or cortical suppressive influences (spared circuits strengthen/ make new connections)= spasticity (inc muscle tone= colnus)
  3. Loss of fine finger movements
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34
Q

What is Parkinsons Disease?

A

degeneration of neurones in the substantial migration + loss of their excitadory (dopaminergic) input of corpus stratum
=loss of activation of focused motor activites, hypokinesia (rigidity, tremors, slow, difficulty make voluntary movements)

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35
Q

What is Huntingtons Disease?

A

Hereditary, rare, progressive + fatal
Loss of caudate, putamen + globus pallid us
= hyperkinesia, dementia, personality disorder, chorea (spontaneous, rapid flicks)

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36
Q

What are names of the congenital condition where the neurotube doesn’t close?

A

Exencephaly- anterior neuropore fails to close
Craniochischisis- fails to close along neuroaxis
Encephalocoele
Spina Bifida- caudal tube fails to close

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37
Q

What is Spina Bifida? What are the 2 subclassifications?

A

Defective closure of the neural tube at the caudal end so vertebral arches don’t fuse
1. Occulta- Failure of 1/2 of arches to fuse (L5 + 6 most common) healthy clinically: small tuft of hair at site. Diastematomyelial (split chord)
2.Cystica- Protrusion of spinal chord +/- meninges through defect in vertebral arches
A- +meningocele- mildest, meninges + CSF
B- + meningomyelocle- nerve roots +/- spinal chord (loose sensation of muscle, paralysis)
C- Myeloschisis (spinal chord open)

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38
Q

What congenital defect does ZIKA virus cause?

A

Microephaly- Imparement/ motor delay/ seizures/ balance + coordination problems

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39
Q

Has a transmitter

A
  1. Synthesis + packaging of neurotransmitter in presynaptic terminals
  2. Na+ AP invades terminal
  3. Activates V gated Ca channels eg./ spider toxins block all here= paralysis
  4. Triggers Ca dependent exocytosis of pre-packaged vesicles in transmitter eg./B.toxin blocks-can stop spasm
  5. Transmitter diffuses across cleft and binds to ionitrophic +/ metabolic receptors
  6. Presynaptic autoreceptors inhibit further transmitter release eg./ activate presynaptic inhibitory receptors
  7. Transmitter is usually inactivated by extracellular breakdown
  8. Transmitter metabolised within cells
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40
Q

Is acetylcholine a neurotransmitter?

A

Yes

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41
Q

What neurotransmitters are monoamines? What is their pharmacological use?

A
  1. Noradrenaline-antidepressants
  2. Dopamine
  3. Seratonin- antidepressants, migranes
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42
Q

What neurotransmitters are amino acids? What is their pharmacological use?

A
  1. Glutamate (fast EPSP)
  2. GABA (Fast IPSP)- antiepilespy/anxiety
  3. Glyceine (fast IPSP)
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43
Q

What neurotransmitters are purines?

A

ATP

Adenosine

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44
Q

What neurotransmitters are neuropeptides?

A

Endorphins
CCK
Substance P

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45
Q

Why is Nitride Oxide an unorthodox neurotransmitter?

A

It is not packaged into vesicles

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46
Q

What is the function of Dopamine + how does this relate to Parkinsons disease?

A

Dopamine has 5 G-Protein coupled receptors (can’t invoke EPSP/IPSP) so has many effects in different regions
Parkisons- degeneration of dopamine in nigrostriatal pathway (S.N- C.S)= stiffness, slow movements, change in posture + tremor
Action-
Brainstem- nausea/ vomit
Basal Ganglia- voluntary movement
Limbic + Frontal- emotion/ rewards
Can’t give dopamine injections as doesn’t cross BBB so need to give Dopamine precursor (make remaining cells produce more) eg./ levodopa + dopa-decarboxylase inhibitor
Dopamine Agonist eg./ ERGOTS (dirty- fibrosis of lung, heart + renal) NONERGOT
Enzyme inhibitors eg./ Peripheral AAD Inhibitors, MAO B Inhibitors (antidepressants); COMT Inhibitors (dec metabolism of Dopamine)
These help tremor, rigidity + bradykinesia but worsen psychosis + nausea
Dopamine antagonist (worsen parkinson’s but stop nausea/ vomitting)
Anticholinergics (tremor)

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47
Q

What is insomnia?

A

Chronic inability to obtain the necessary amount/ quality of sleep to maintain adequate daytime behaviour
A- Chronic, primary, no cause
B- Temporary, secondary to pain physical/ emotional
NOTE: very difficult to see on electro encephalogram (EEG)
Treat with Benzodiazepines (addictive)

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48
Q

What is somnambulism?

A

Sleep walking- delta sleep (S4) no recollection

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49
Q

What is Narcolepsy?

A

Directly into REM, accidental risk. Due to innappropriate melatonin release from hypothalamus

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50
Q

How can you damage CN1?

A

Fracture to cribriform plate may tear olfactory nerve fibres

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51
Q

How can you damage CN2?

A

Optic
Papillodema- Inc CSF, blood can go out but not back (pools in optic cup)= damage to nerve/ chasm/ tract
Vision Problems eg./ short vision= demyelination of nerve
Optic Neuritis- Demyelination of optic nerve giving monocular vision loss, pain on movement, reduced visual acuity/ colour vision, optic disk swollen (MS association)

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52
Q

How can you damage CN3, 4 + 6?

A

Occulomotor, Trochlear + Abducent
Cocaine, Youth, Dim Light (parasympathetic nerve damage), Anxiety, Brain Death, Anxiety/ Excitement, Old Age, Bright Light (sympathetic chain damage), opiate overdose, Horners Syndrome, Isolated/ Combination Nerve Palsy, Diplopia die to muscle deviations,Supranuclear Nerve Palsy (eg./ parksinsons)

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53
Q

How can you damage CN5?

A

Trigeminal
Trigeminal Neuralgia- Paroxysmal attacks of pain, triggers, middle aged/ older due to compression of nerve in posterior fossa.
Treat with carbamazepine/ surgery if resistent

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54
Q

How do you damage CN 7?

A

Facial
Long path through bone so injury most common
Bells Palsy- unilateral facial weakness, idiopathic, LMN (loose forehead movement), preceded by pain in ear, eye closure affected (risk of corneal damage). Treat with steroids _ lubricant

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55
Q

How do you damage CN8?

A

Vestibulocochlear
Vestibular Neuronitis- sudden onset of disabling vertigo + vomit, gradual recovery ( no known cause)
Nystagmus- congenital/ visual/ peripheral/ brainstem/ cerebellar/ toxins (alcohol, phenytonin- anti epileptic)

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56
Q

How do you damage CN 9+10?

A 
Glossopharyngeal + Vagus
Bulbar Palsy (LMN)- polio, tumours, syphilis= dysarthria (slurring), dysphagia, dysphonea, wasted fasciculated tongue
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57
Q

How do you damage CN 12?

A

Tonsillectomy

Tip deviates to AFFECTED side

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58
Q

What happens when Cerebral Perfusion Pressure >150mmHg?

A

Autoregulation fails (50-150mmHg) so contraction of arterioles no longer sufficient to maintain constant blood flow to brain.
= Hypertensive Crisis- vasogenic oedema
eg./ toxins eg./ CO2, first 4-5 days of head trauma

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59
Q

What are the 3 different types of cerebral oedema?

A
  1. Vasogenic Edema- Extacellular (Inc capillary permeability) Fluid is plasma (protein) infiltrate due to tumour, infarct, abscess, trauma. Treat via mannitol + steriods
  2. Cytotoxic-Intracellular Fluid in water + sodium due to failure of membrane transport. Treat via mannitol
  3. Interstitual- Hydrocephalus impared CSF absorption (obstructing/ non-obstructing)
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60
Q

What is persistent vegetative state?

A

Brain stem recovers to a considerable extent but no recovery of cortical function (lost content of consciousness) but not ascending so awake

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61
Q

What is locked-in syndrome?

A

Total paralysis below 3rd nerve nuclei ( open eyes, look up and down, smell) Damage to front of pons (stroke in basilar artery) where pyramidal tracts cross so can’t move arms/legs

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62
Q

How do you treat a Pt in coma/ persistent vegetative state/ locked-in syndrome?

A 
Airways
Breathing
Circulation
Bloods, BP, Pulse, Temp, IV Acsess
Meningitis?
GCS
CN Tests
Motor Function- tone, reflex
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63
Q

A Pt presents in a coma GCS

A 
Toxicology
Blood Sugar + Electrolytes
Heaptic + Renal Function
Acid-Base Assesment + Blood Gasses
BP
CO (poisioning)
Could be-
DKa, Metabolic (acidosis/ alkalosis), Alcohol/ Drug Overdose, Epilepsy, Infection, Medical (Diabetes, sepsis, renal/ hepatic failure)
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64
Q

A Pt presents in a coma GCS

A 
CT Head Scan
LP- Appearance, Cell Count, Glucose levels
Could be-
Meningism
Subarachnoid Haemorrhage 
Encephalitis
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65
Q

A Pt presents ina coma, GCS

A

CT/MRI
Metabolic Screen
Lumbar Puncture
Electro Encephalogram (EEG)

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66
Q

What group of individuals is at the highest risk of coma? What is the curators marker for a ‘good outcome’ if Pt wakes before?

A

Young as brain hasn’t shrunk yet

6 hrs is marker for ‘good outcome’

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67
Q

What are the 4 types of head injury and how are they managed?

A
  1. Diffuse Axonal Injury (multiple lesions, accel/deceleration trauma, cause of PVS)
  2. Contusion
  3. Intracerebral Haematoma
  4. Extracerebral Haematoma
    - extradural= convex on CT
    - subdural= concave/ convex on CT
    Treat via ABC, CT, stablize cervical spine, intubate + ventilate (if GCS
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68
Q

What is a stroke and what are the 2 types?

A

Sudden onset of focal/global neurological symptoms lasting >24hrs

  1. Ischaemic- Atherothromboembolism (carotids), small vessel occlusion (lacune), cardiac emboli (AF, endocarditis, MI)
  2. Haemorrhagic- Intracerebral Haemorrhage, subarachnoid haemorrhage, AV malformation
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69
Q

What is different about strokes in young people?

A

Sudden BP drop
eg./ boundary/watershed stroke (area between 2 vascular beds), carotid artery dissection , subarachnoid.haem, thrombophilia

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70
Q

What is the pathology behind a stroke?

A

Failure of cerebral BF- Degree of Hypoxia (brain doesn’t have energy supply)- Prolonged- Anoxia (no 02)- Infarct (cell death at 10mL/100gtissue/min) - Necrosis= oedema/ swelling/ secondary haemorrhage

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71
Q

What are the risk factors for a stroke?

A

Smoking
Alcohol
High Fatty diets (lipids + cholesterol- atherosclerosis)
Hypertension (haemorrhage + lacunar)
Oral Contraceptive
Diabetes Mellitus
Hypercoagualbility
Impaired cardiac function (previous episode)
Small Artery Lipohyalonosis (thickening= Dec luminal diameter= lacunar stroke)

72
Q

What are the symptoms when a stroke affects a cerebral artery?

A
  1. Anterior Cerebral- Frontal + Parietal. Contralateral paralysis + sensory loss of foot + leg, gait impairment.
  2. Middle Cerebral- paralysis + sensory loss of face/arm/leg, homonymous hemianopia (gaze deviates towards stroke), aphasia (if LHS-Wernicks), unilateral neglect + agnosia
  3. Posterior Cerebral- usually basilar. Coma, vertigo, nausea, vomiting CN palsy, ataxia, hemiparesis, hemisensory loss
73
Q

What are the 4 classes of strokes?

A
  1. Total Anterior Circulating Stroke- TACS
  2. Partial Anterior Circulating-PACS
  3. Lacunar (small vessel)-LACS
  4. Posterior Circulating Stroke- POCS
74
Q

A Pt comes in with Face dropping to one side, loss of Arm movement and Speech slurred. What is your clinical diagnosis and how do you determine this?

A 
Fast
Bloods- FBC, Glucose, lipids, ESR
CT/ MRI Head
Echocardiogram (AFIB, LVH)
Carotid Doppler (stenosis)/ Angiogram
75
Q

What is your acute management of a stroke?

A
  1. Protect Airway
  2. Investigations (pulse, BP, BGL, ECG, CT/MRI, thrombolysis if onset <4.5hrs)
  3. Antiplatlets agents eg./ Tissue Plasminogen Activator (ischaemic only)
76
Q

What is a transient ischamiec attack?

A

TIA
Symptoms resolve within 24hrs, can precede a stroke
= carotid bruit, Inc BP, heart murmur (valve disease, AFIB), retinal artery emboli (fundoscopy).
Same tests as stroke (FBC, glucose, lipids, ESR, CT/MRI, doppler/ angiography)
Treat via controlling risk factors, antiplatlets eg./ clopidogrel, warfarin (AF, stenosis, MI),
Carotid Endarterectomy
NOTE: cant drive for 1 month

77
Q

What is dementia?

A

Syndrome (clinical diagnosis) with progressive impairment of multiple domains of cognitive function. Leads to loss of acquired skills and interference in occupational and social roles

78
Q

What causes dementia?

A
  1. Alzheimers (late/early onset)
  2. Vascular Dementia (early onset, stepwise profession of many small strokes)
  3. Lewy Body Dementia (late onset visual hallucinations- parkinsonism syndrome)
  4. Fronto-temporal (atrophy)
  5. Others eg./ alcohol, Huntingtons, HIV, MS, syphilis
79
Q

How is dementia diagnosed and managed?

A

Is a clinical syndrome so diagnosed by clinical signs

  1. History (independent witness)
  2. Exam- Cognitive Function, Neurological, Vascular, MiniMental State Exam, MOCA
  3. Bloods, CSF, EEG, CT/MRI, biopsy

Refer to specialist memory service
Acetylcholinesterase inhibitors
SSRI- Depression
Rivastigmine (levy body as antipsychotics can worsen side effects)
Antiglutamatergic Treatment
Folic Acid + B Vitamins- decrease mild cognitive decline

80
Q

What is Alzheimers?

A

Enduring, Progressive + global (most dementias only affect one area) cognitive impairment.
Lose visuospatial skills; memory; verbal ability; executive function; agnosia; mood/ behavioural disturbance in progressive disease, psychosis.
Caused by genetic(familial AD + Downs link) + βamyloide peptide accumulation destroys neuronal cells, acetylcholine loss + Environment (Diabetes, Depression, Smoking)
Treatment is same for dementias
NOTE: targeting βamyloid doesn’t seem to work

81
Q

What is Parkinsons?

A

65y/o onset. Bradykinesia (slow to initiate movement), Ridgicity/Tone + Tremor, Postural Instability (clinical syndrome so >+2= parkinson’s Diagnosis)
+ loss of sense of smell, constipation, hallucinations, urgency
Cause: Idiopathic, Drugs (eg./ schitzophrenia), Vascular (stroke in BG, cerebellum, pyramidal tracts), Encephalopathy
Pathology: mitochondria DNA dysfunction causes degeneration of dopimergic neurones in SN= Dec Dopamine levels (dopamine good symptomatic treatment)
Investigate: Dopamine Transporter SPECT (loose tails of putamen)

82
Q

How do you treat Parkinsons?

A

Can’t treat disease can only treat clinical manifestations/ symtoms

  1. Levodopa + dopa-decarboxylase inhibitor. Efficacy reduces with time
  2. Dopamine Agonist +MOA-B may delay need for levodopa
  3. Anticholinergics help tremor but can cause confusion
  4. COMT Inhibitors- stop doses wearing off, hepatic dysfunction
83
Q

What is a glioma? What are the classifications?

A

Primary (benign- diffuse edges, non operable. malignant- not mets outside CNS) Brain Cell Cancer

  1. Embryonic Neural Cells (neuroectoderm)- Medulloblastoma- kids, hard to operate (posterior fossa), undifferentiated cells.
  2. Astrocytoma- low grade, slow growing, small cell
  3. Glioblstoma (multiforme, from astrocytes)- atypical, necrosis, quick, large cell.
  4. Oligodendrocytes- Oligodendroglioma
  5. Ependymal Cells (line ventricles)- Ependymoma
84
Q

What is a Meningioma? How does it form?

A

Arachnocytes (arise from arachnoid)- slow growing, benign, compressive, can’t resect- bland cells forming small groups +/- calcification

85
Q

Where are nerve sheath tumours? How can they clinically present?

A

Around peripheral nerves
Schwannoma/ Acoustic Neuroma
CN8 affected (unilateral deafness)
benign but removal difficult

86
Q

What is a CNS Lymphoma

A

Lymphoid Cells

eg./ Diffuse large B-Cell Lymphoma

87
Q

What is a haemangioblastoma?

A

Tumour of BV

May bleed

88
Q

What areas commonly metastasise to the brain?

A

Lungs
Breast
Kidney
Colon
Melanoma
Find via CT chest/abdo/pelvis, mammography, biopsy
NOTE: No LP when signs of raised ICP, mass lesion (CT before as herniation due to pressure drop is possible)

89
Q

What clinical features can Inc ICP cause in relation to cranial nerves and brain herniation

A

Papillodema
3rd + 6th Cranial nerve palsy
R-L/L-R shift= subfalcine, Lateral V crushed
Uncal Herniation= over edge of tentorium, aqueduct narrowed
Coning= cerebellar tonsils into foramen magnum, coma, brain death

90
Q

What differentiates an UMN from LMN?

A

UMN- Anterior Horn + Above

LMN- Distal to Anterior Horn

91
Q

Is Weakness UMN or LMN?

A

Both

92
Q

Is Muscle Atrophy UNM or LMN?

A

LMN

93
Q

What is the difference in reflexes between UMN and LMN?

A

UMN- Reflexes increased (hyperflexia)

LMN- Reflexes decreased

94
Q

What is difference in tone in UMN vs LMN?

A

UMN- Increased

LMN- Decreased

95
Q

Is fasciculation’s UMN or LMN?

A

LMN

96
Q

Is Babinski sign seen in UMN or LMN?

A

UMN

97
Q

What is Cauda Equine Syndrome?

A

Spinal chord runs from C1-L2 so compression of nerve roots after L2- Cauda Equina Syndrome= herniation of lumbar vertebrae via tumours, abscess + bleeding.
presents as bilateral sciatica (shooting pain), saddle anaesthesia + urinary dysfunction
URGENT MRI- lumbar disectomy

98
Q

How does a disk Prolapse occur? How dies it present?

A 
Acute Herniation (posterolaterally) of IV disk causing compression of spinal roots (LMN) or spinal chord (UMN).
Presents with sciatica (shooting pain down leg), numbness + weakness
MRI- rehab, steroid injections, lumbar/cervical disectomy.
99
Q

What is cervical spondylosis?

A

Degenerative change in cervical spine (spine + nerve root compression)
Myelopathy +/- radiculopathy
Long Onset
Surgery if late stage/ myelopathy (weak, clumsy, no dexterity)

100
Q

What is lumbar spinal stenosis? How does present?

A

Disk compression of ligaments (all nerve roots getting squashed)
Spinal Claudication (pain down both legs), worse on walking/ standing, relieved on sitting.
Manage with lumbar laminectomy

101
Q

What is an epidural abscess? How is it caused + how do you diagnose it?

A

Infection in epidural/ extra dural space
presents as back pain, pyrexia + focal neurology- URGENT MRI + surgical decompression + long term IV antibiotics (as of don’t remove become paraplegic)

102
Q

What is osteomyelitis? What can cause it? How can it be treated?

A

Infection within vertebral bodies via Chronic Renal Failure, Alcoholism, Drugs, Diabetes, AIDS
Give antibiotics + surgery

103
Q

What spinal level is check by specific myotomal stimulation?

A

Elbow flexors/ extensors= C5/7
Wrist Extensors= C6
Finger Extensors= C8
Hand Muscles= T1

Hip Flexors= L2
Knee Extensors= L3
Ankle Dorsiflexors= L4
Long Toes Extensors=L5
Ankle Plantar Flexors=S1
104
Q

What 3 things are rehabilitation based upon?

A
  1. Imparement
  2. Disability/ Activity Limitation
  3. Handicap/ Participation Limitation
    Rehab= restoration of Pt to their fullest physical, mental + social capactiy
105
Q

What is meningitis?

A

Inflammation/ Infection of the meninges
Presentation: Fever (>38), Meningism (neck stiffness, photophobia, nausea, vomitting), altered mental state, petechial rash (non-blanching)
Cause:Infective (bacteria eg./ neissaria meningitis, strep. pneumonia); Infective (eg./ sarcoidosis); Viral (eg./ enterovirus); Drugs (NSAIDS); Mets; Lymphoma/ Myeloma/ Leukaemia

106
Q

How do you investigate + treat meningitis?

A

Medical Emergency
Investigate: via blood culture + lumbar puncture (after CT/ GCS 15)
1. Give benzylpenicillin (if acute presentation)
2. ABC + fluid + cefotaxime post LP (+ampicillin if >55)/ Aciclovir if viral suspected
3. Dexamethasone, 30degree heat tilt
Possible adjustment to antibiotic therapy when lab results return

107
Q

How can you usually tell a bacterial from viral with respect to a meningital/ enchephalital lumber puncture?

A

High opening Pressure + high Cell Count (polymorphs, neutrophils) + Low Glucose + High Protein= bacterial
Normal opening pressure + low Cell Count (lymphocytes) + Normal Glucose (60%BGL) + Slightly Elevated Protein= Viral

108
Q

What is Encephalitis?

A

Inflammation/ Infection of Brian substance
Flu like, Decreased consciousness, progressive headache +/- menignism, cerebral dysfunction, seizures, focal (1sided)
Cause: Viral (eg./ HSV give aciclovir); hypoglycaemia; hepatic encephalopathy, DKa, hypoxic brain injury; immune (anti-VGKC frequency seizures + amnesia); animal bite

109
Q

How do you investigate and treat encephalitis?

A 
Investigate:
Bloods (cultures- serum/ viral PCR)
Contrast Enhanced CT (Meningeal enhancements= meningoencephalitis; bilateral temporal lobe lesion=HSV cause)
LP (inc protein + lymphocytes, dec glucose)
EEG
Treat: 
Aciclovir (adjust according to eGFR)
Phenytoin (for seizures)
110
Q

What is the difference between abscess and empyema and how would a Pt present?

A

Abscess- localised area of pus within the brain (walled off)
Empyema- thin layer of pus between dura + arachnoid membrane (sub/extradural)
Clinically- Raised ICP (papilodema, CN palsy if herniation); Fever; Headache
Tends to come from infection spread eg./ otitis media
Investigate via CT/MRI, blood culture
Treat: Biopsy + drain pus, if strep (penicillin) if anaerobes (metronidazole)

111
Q

What affect can HIV have on the brain?

A

Test via india ink/ toxoplasmosis serology

Inhaled in lungs- crosses BBB- meningioencephalitis

112
Q

What affect can Lymes disease have on the brain?

A 
Borrelia Burgdorferin
Early Infection (bulls eye lesion)- Disseminated Infection- Chronic (encephalitis, encephalomyelitis)
113
Q

What organism is syphilis? What affect can it have on the brain?

A

Treponema Pallidum

Tertitary Stage= neurosyphilis (rare)-give high dose penicillin

114
Q

What is Creutzfeldt- Jakob Disease (CJD)?

A

Rapidly progressive dementia
myoclonus, ataxia, weakness, spasticity etc
new variant <40

115
Q

What is Virkows Triad made up of?

A
  1. Stasis of Blood Flow (decreased BF/Inc BP= burst vessels)
  2. Hypercoaguability (thrombosis, bleeding due to anticoagulation, reduced platelets + clotting factors)
  3. Endothelial Injury (vessel wall via atheroma/ vasculitis/ outside pressure)
116
Q

What is the main cause of interrupted blood supply?

A

Atheroma + Thrombus- Ischemia
Anoxia (10mL/100g/min) for >3mins= Infarction- damage to neurones + cells permanent- foamy macrophage infiltrate- cysts/ loss of brain tissue

117
Q

Where does a thrombus usually occur in the heart? How can this affect the rest of the body?

A

Stagnation of blood in appendages due to A.Fib-pushed out- arm (digital infarct); kidney (haemoturia); legs (claudication); carotids _ vertebral (ischemic stroke)
Risk Factors: Thyrotoxicosis, Ageing, Carcinoma eg./ brachial, Sympathetic inc eg./ alcohol, cocaine etc

118
Q

Aneurysms and the brain

A

Ruptures- haemorrhage
Cerebral arteries have thin walls and no muscle so won’t constrict no matter the change eg./ caffeine, angiotensin) won’t constrict so no affect on cerebral blood flow
Thin Wall- Weakening(hypertension)- Rupture (haemorrhage + bleed) shown via spasm of artery
eg./ Basal Ganglia microaneuryms in hypertensive Pts (loose tracts), inoperable
eg./ Berry aneurysm in CofW if hypertensive IS amenable to surgery (clip)

119
Q

What kinds/ types of problems can be classified as hypoxia?

A
  1. Hypoxia with intact circulation (eg./ CO poisoning, drowning, respiratory arrest, dec 02 levels)
  2. Inadequate blood supply eg./ cardiac arrest, hypotension, cardiac arrest- necrosis as no perfusion, coronory artery disease.
  3. RARE- inability to use 02 eg./ cyanide poisioning
120
Q

What is a primary headache?

A

No underlying medical cause- tension headaches (most common), migraines + medication overuse

121
Q

A Pt presents with
Bilateral, pressing + scalp muscle tenderness with no nausea or sensitivity to head movements.
What kind of headache do you think they have? How do you determine its frequency?How could you treat this?

A 
Primary: Tension Type Headache
<1day/ month= infrequent 
1-14d/m= frequent
>+15d/m= chronic
Treat with stress relief + antidepressants/ pain killers eg./ NSAIDS
122
Q

A Pt presents with
Aura followed by unilateral throbbing headaches with nausea, vomiting + photophobia
What kind of headache do you think they have? What is the pathology occurring?

A

Primary: Migrane
Don’t have habituation so factors (alcohol, sleep dehydration, exercise etc) act on hypothalamus and change cortisol responsiveness - hyperexcitability activates trigeminal ganglia- recurrent pain pathway circuit (brainstem, neuropeptides + meningeal involvement)

123
Q

What are the stages of a migraine?

A
  1. Premonitor- Warning via food cravings, mood changes, fatigue, cognitive changes, muscle pain, fluid retension.
  2. Aura (1/3)- Fully Reversible
    - Visual- scotmoma, hemianopia
    - Senosry-parathesia
    - Motor- hand + arm on one side
    - Brainstem- quadraphalgia, loose conscious
  3. Early Headache- Mild (dull, nasal congestion, muscle pain)
  4. Adv. Headache- Severe (unilateral throbbing, nausea, vomiting, photophobia, photophobia)
  5. Postpone- Resolution (fatigue, muscle pain, cognitive changes)
124
Q

How do you treat a migrane?

A
  1. NSAIDS
  2. Triptains (5HT agonists)
  3. Propanolol (BP)
  4. Amitriptaline- antidepressants
125
Q

What kinds of things are triggers for migraines?

A 
Chocolate
Hangovers
Orgasms
Cheese
Oral Contraceptives
Lie ins
Alcohol
Tumult
Exercise
126
Q

How is a medication overuse headache classified?

A

> +15days due to opiates, cholinergics, caffeine (gets worse on normal medication)
Can start in pregnancy (cant give anti epileptics as teratogenic)

127
Q

What are the 4 trigeminal autonomic cephalalgias?

A
  1. Cluster Headache
  2. SUNCT
  3. Paroxysmal Hemicrania
  4. Trigeminal Neuralgia
128
Q

A Pt presents with-
Rapid onset of excruciating pain around 1 eye (watery + bloodshot); facial swelling; nausea + vomit; photophobia + phonophobia.
These attacks can last 15-180mins and can be up to 8 times per day.
What is your clinical diagnosis and how would you treat this?

A

Cluster Headache
Carry 02 and sumatriptan for acute attacks
+ steroid injections as a preventative

129
Q

A Pt Presents with-
Stabing, burning head pain
Unilateral orbital pain + lacrimination.
Triggered by could, touch, chewing, wind.
What is your clinical diagnosis and how would you treat this?

A

SUNCT
No abortive treatment but can use carbamazepine as prophylaxis
Get 3-200 per day lasting 5- 240 seconds

130
Q

A Pt presents with-
Paroxysms of intense, stabbing pain in maxillary/ mandibular region lasting 5-10s between 3-200 times per day.
What is your clinical diagnosis and how would you treat this?

A

Trigeminal Neuralgia
Prophylaxis- carbamazepine, phenytoin, gabapentin
Surgery- decompressive, glycerol ganglion injection, stereotactic radiosurgery

131
Q

What are Red Flags for headaches?

A

Sudden change in frequency/ characteristics/ associated symptoms
localises to 1 area/ side
neck stiffness/ fever (thing meningism)

132
Q

How are bruises formed?

A

Blunt force to skin and tissues- damages little blood vessels- blood oozes into subcutaneous tissues + muscles
eg./ perioribtal contusions (black eyes) as blood tracts down and pools in orbital ridges

133
Q

What is an abrasion/ graze?

A

Injury to superficial part of skin- sore/ bleed but heals without scarring
eg./ scratch

134
Q

What is a laceration?

A

Blunt trauma, need to explore for foreign bodies

eg./ fall, tear, split

135
Q

What is an incision?

A

Sharp, caused by cutting force
Energy (lots) delivered over a small area
eg./ knie, glass

136
Q

What are the different types of fracture?

A
  1. Ring Shaped- continues fracturing as huge force travels out.
  2. Fissure- Less energy dissipated from point of impact (not enough to complete ring)
  3. Depressed/Sign- Piece of bone pushed inwards by application of force/ injury. Usually localised (leaves shape of object)
  4. Hairline- Barely visible, requires no treatment but may be portal for infection
137
Q

Where is an extradural haemorrhage? What happens?

A

Also called epidural
In area between skull + dura due to bleeding meningeal arteries/ tear in dural venous sinus.
Initial Drowsiness- Loss of consciousness after a few days (dropping GCS due to rising ICP) + severe headache, fits, vomiting, hemiparesis, breathing deep and irregular (brainstem compression)- Death (respiratory arrest)
Tests- CT
Manage- clot evacuation and ligation of vessel

138
Q

Where is a subdural haemorrhage? What happens?

A

Blood between dura + arachnoid happens as brain moves at different speeds to dura. If go in opposite direction/ different speeds eg./ trauma, mets then bridging veins tear- Inc venous pressure.
NOTE: elderly and alcoholics have more brain shrinkage so more likely to tear
Uncal Herniation/ Coning possible
Clinically- fluctuating consciousness, personality change
Test-CT
Manage- irrigation via craniostomy/ craniotomy

139
Q

How do you tell an extradural to subdural haemorrhage apart on a CT?

A

Subdural is sickle (c) shaped

140
Q

What is a subarachnoid haemorrhage? What happens?

A

Blood between arachnoid + pia caused by sudden movements of head with acceleration and rotational component- vertebral artery damage/ rupture of saccular aneurysm
Presents as a thunderclap headache (sentinel warning headache), neck stiffness, tersons syndrome (retinal, subhyaloid and virtuous bleeds)
Test- CT, LP (>12hrs for bilirubin breakdown)
Treat- coil/ clip aneurysm

141
Q

What is a intracerebral haemorrhage? What happens?

A

Natural causes eg./ hypertension, elderly, vascular tumours, amyloid antipathy (vessels susceptible to rupture)

142
Q

What is intracerebral cortical contusions?

A

Brain injured by striking inner aspects of skull base
coup (site of damage) and countercoup (where brain moves across skull base and damages opposite end, larger + more prominent)

143
Q

What is diffuse axonal energy?

A

Destruction due to force in brain. Big acceleration/ deceleration force.
= glide haemorrhages in corpus callosum (deep in white matter) Incompatible with life

144
Q

What are the 4 types of aneurysm?

A

Saccular- 1 sided bulging
Fusiform- both sides bulging
False- into adventitia
Dissecting- all layers

145
Q

What posture change is associated with syncope vs seizure?

A

Syncope- upright

Seizure- any

146
Q

A change in pallor is associated with syncope or seizure?

A

Syncope (whitening)

147
Q

Where is incontenece seen? Syncope or seizure?

A

Seizure, unless full bladder then it can happen in syncope

148
Q

What kind of things precipitate a syncopated episode?

A

Light Headed, Nausea, hot/sweat, tinnitus, tunnel vision

149
Q

What is the most common kind of syncope?

A

Vasovagal (cariogenic) most common- due to reflex bradycardia +/- peripheral vasodilation.
Can have colonic twitches (due to cerebral hypoperfusion)

150
Q

What are the 3 most common events precipitating a seizure?

A
  1. Hypoxic Seizures- kept upright during syncope eg./ dentist, aircrafts etc.
  2. Concussive Seizures- instant, after blow to head.
  3. Cardiac Arrhythmias- Abnormaility/ Myopathy makes you more prone eg./ long QT syndrome can cause collapse after injury. Seizures can also cause arrhythmias
151
Q

How do you investigate a seizure/ syncope episode?

A 
Get a good history from person + 3rd party if possible.
Blood Sugars (hypoglycaemia), ECG (arrhythmias), toxicology (alcohol/ drugs), CT Head (1+ event)
152
Q

What is epilepsy?

A

Seizures occurring spontaneously brain activity (grey matter)
J shaped incidence (high babies, low childhood- early adulthood, high in elderly + learning difficulties)
tonic-colonic movements (motor sign of electrical discharge), tongue biting, triggers by flickered lights (photosensitive)
Investigate via- EEG (+hyperventilative + photic + sleep deprivation)

153
Q

What are the 2 types of epileptic seizures? How are they classified?

A
  1. General Seizures- Functional Disorder (FH), Tonic (stiff)- Colonic (jerk), Myclonic (sudden jerk), Atonic ( loss of muscle tone= fall).
  2. Focal/ Partial- Structural Disorder (aura), MRI (scaring), Ct (stroke, tumour, bleed) may evolve to general convulsive.
154
Q

How is driving affected by seizures?

A

If 1 can drive after 6 months + HGV after 5 years if not further events

155
Q

What treatment would you give an epileptic Pt?

A

No drugs after first event- give relaxation treatment and ways to stop aura
Further events
1. Sodium Valproate (tonic-colonic seizures, liver failure and pancreatitis common) use Lamotrigen is child bearing age.
2. Carbamazepine (partial seizures)- sodium valproate- lamotrigen
3. Vigabatrin (infantile spasm)

156
Q

What is status epileptics?

A

prolonged, recurrent, tonic-colonic seizures over 30 mins with no recovery period
Damaged brain cells due to glucose and oxygen demand
Treat via benzodiazepines (eg./ diazepam)- valproate- anasthesia (shut off brain activity)

157
Q

What is the difference between a myelopathy and a radiculopathy?

A

Myelopathy- UMN, stop sensation getting past area eg./ MS, autoimmune, haemorrhage, B12 deficiency, bladder retention and bowel constipation.
Radiculopathy- LMN, root lesion= dermatomal sensory loss

158
Q

What is a spinal chord stroke?

A

Vascular Risk Factors (anterior spinal artery common)
Pain is back/viscera (referred)
Gives numbness + paraparesis, urinary retension.
Treat- OT, Physio, reverse arrythmias, hypertension + antiplatelet therapy

159
Q

What is demyelinating myelinitis?

A

Inflammation of myelin sheath (white matter)
Involved in MS (initial presentation)
treat via supportive/ methyl prednisolone

160
Q

What does B12 have to do with the spinal chord and nervous system?

A

Need B12 for normal chord and peripheral nerve function (absorbed from gut via intrinsic factor from gastric parietal cells)
Stopped by pernicious anaemia (autoimmune), chrons, gastrectomy etc.
Myelopathy, peripheral neuropathy, cognitive dysfunction- dementia, optic nerve- blindness.
Treat- IM B12

161
Q

What is Multiple Sclerosis? What is the aetiology and risk factors involved?

A

Autoimmune inflammatory condition of CNS- Demyelination of white matter
TCells-Cross BBB- Attack myelin sheath- Acute inflammation + demyelination= Post-inflammatory gliosis(hypertrophy) + Axon loss= loss of function
Risk Factors: Genetic (FH of other autoimmune), Autoimmune, Female, Epstein Barr Virus

162
Q

What is optic neuritis?

A

Pain, Vision Loss/ Colour, optic disk swells, pupillary defect resolves over weeks.
Symtom of MS, B12 deficiency

163
Q

How does MS present?

A

Initial Attack (20s, gradual)-Progressive
- Resolve/ Recovery
Further Relapse
Progressive Stage
Myelitis (inflammation within the spinal chord)

164
Q

What can cause inflammation within the spinal chord?

A
  1. Late stage MS (myelitis)
  2. Sarcodosis
  3. Infection eg./ lames, encephalomyelitis
165
Q

What complications occur with MS/ a progressive attack?

A 
UMN
Unilateral Optic Neuritis/ Diplopia/ Nystagmus
Stiffness/ Spasms/ Spasticity 
Loss balance/ speech/ slurred
Bladder + Bowel
Memory Loss/ dementia
Trigeminal Neuralgia
166
Q

A 45 year old Pt presents with double vision, pain, loss of balance + cognitive function, urinary + bowel change and recent onset memory loss after having a loss of consciousness last week.
They have a PMH of this type of attack in their 20s where they lost function of their limbs. What is their most likely clinical diagnosis? How could you prove this and what would you do next?

A

Further relapse of Multiple Sclerosis (1st incidence in 20s)
Investigations:MUST be to McDonald Criteria (disseminated in time-LP + space-MRI)
MRI (T1 + Gadolinium to see acute lesions); LP (oligioclinal bands of inflammation in CSF); Chest-Xray, Bloods (rule out other autoimmune eg./ sarcoidosis, test for other cause eg./ Vit B12 dysfunction)

167
Q

How do you treat MS?

A

Encourage a mediterannian diet, stress free life
If acute relapse- look for infection and give oral/ IV methylprednisolone
Reduce Relapse Rate- Interferons, monoclonal antibodies, non- immunosuppressants
Symptomatic Treatment- Amitriptyline , laxatives, Botulinum Toxin, self catheterisation

168
Q

What types/ progression of MS can occur?

A
  1. Relapse Remitting
  2. Secondary Progressive
  3. Primary Progressive
  4. Sensory (mild sensory disturbance, no disability)
  5. Malignant (fast, extensive disability)
169
Q

What is the different between mononeuropathies and polyneuropathies?

A

Mononeuropathies eg./ carpal tunnel syndrome lesions of individual peripheral/ cranial nerves BUT can be mono neuritis multiplex (multiple nerves)- systemic eg./ Diabetes Mellitus
Polyneuropathies- disorders of cranial/ peripheral nerves whose distribution is symmetrical and widespread

170
Q

What is a common mononeuropathic disease? How is it treated?

A

Ulnar mononeuropathies from entrapments (5 common places in ulnar nerve- epicondylar groove most common)
Treat via rest + avoidance of pressure on the nerve. If extreme pain elbow splinting (prevents flexion)

171
Q

What is motor neurone disease?

A

Selective loss of neurones in the motor cortex, cranial nerve nuclei + anterior horn cells.
UMN + LMN are affected but there is no sensory loss/ sphincter disturbance/ eye movement disturbance

172
Q

What are the 4 clinical patterns of MND? How do you treat them?

A
  1. ALS/ Amyotrophic lateral sclerosis- loss of motor neurones in the motor cortex + anterior horn cells= weakness, UMN signs (babinski), LMN atrophy
  2. Progressive Bulbar Palsy- affects CN9-12
  3. Progressive Muscular Atrophy- Anterior horn cell lesion (UMN signs)
  4. Primary Lateral Sclerosis- Loss of Beta Cells (motor cortex)- no cognitive decline but UMN signs
    Treatment- MDT. Antiglutamtergic drugs, amitriptyline (drooling), NG tube, opioids, non-invasive ventillaition
173
Q

A 40 year old Pt presents with a stumbling gait, foot drop , proximal myopathy, weak grip and aspiration ammonia
What is you clinical suspicion. How do you confirm this?

A

Motor Neurone Disease
Look for UMN (spasticity, brisk reflexes, babinski) and LMN signs (wasting/ fasciculation of tongue, abdomen, back + thigh) + Bulbar Signs (speech/swallowing affected)

174
Q

What is Myasthenia Gravis? How do you treat it?

A

Autoimmune antibodies to nicotinic acteylcholine receptors (AChR) interfering with NMJ transmission
= Inc muscular fatigue, diplopia, myasthenia snarl on smiling
Test: AChR Antibodies, EMG, CT thymus
Treat: Anticholinesterase, Immunosuppression (prevent relapses) eg./ prednisolone, Steroids, thymectomy

175
Q

What is Myasthenia Crisis?

A

Weakness of the respiratory muscles (during a relapse) treat via plasmapheresis + treat relapse trigger eg./ infection

176
Q

What is Guillain Barre Syndrome?

A 
A symmetrical descending muscle weakness a few weeks after infection (antibodies attacking nerves)
Autonomic Dysfunction (sweating inc pulse, arrhythmias, BP change, pupil contraction) Slow nerve conduction, LP (Inc Protein)

Neurology (3 decks)

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