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Phase 3a Finals > New Neurology > Flashcards

New Neurology Flashcards

1
Q

What is presbycusis?

A

Age related sensorineural hearing loss

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2
Q

What is Otosclerosis?

A

autosomal dominant replacement of normal bone with spongy vascular bone.

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3
Q

What is menieres disease?

A

Recurrent episodes of vertigo, tinnitus and sensorineural hearing loss, lasting mins-hours. Vertigo main complaint!

Middle aged adults
Feeling of aural fullness/pressure
Nystagmus/positive romberg test

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4
Q

Investigations in Meniere’s disease

A

Menieres triad
- Otoscopy - Normal ear drum
- Audiometry - Sensorineural hearing loss
- Tympanometry - normal

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5
Q

Pharmacological mx of menieres

A

Prochlorperazine (acute vertigo and nausea) [Acute attacks]
Betahistine medication (H1 agonist that acts as a Vestibular sedative) [Prevention]
Intratympanic gentamicin injection if surgical

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6
Q

What is Acoustic Neuroma?

A

AKA vestibular schwanomma. Tumour arising from schwann cells myelinating CN8. Usually presents between 40-60yo.

Associated with type 2 neurofibromatosis

Presents similar to menieres (vertigo, tinnitus, S hearing loss) BUT also has absent corneal reflex and possible facial paralysis

Affected cranial nerves:
- Men. symptoms (VIII)
- Absent corneal reflex (V)

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7
Q

How can acoustic neuroma present?

A

Depends on cranial nerves affected
- CN5: Absent corneal relfex
- CN7: Facial palsy
- CN8: Unilateral sensorineural hearing loss and tinnitus, vertigo.

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8
Q

Ix of Acoustic Neuroma

A

Audiogram and examination show sensorineural hearing loss.

MRI Gold standard imaging for diagnosis and tumour tracking.

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9
Q

Mx and comps of acoustic neuroma

A

Conservative or
Tumour excision or
Radiotherapy
Permanent hearing loss (CN8), permanent facial weakness (CN7)

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10
Q

What is an essential tremor, give features and management?

A

Autosomal dominant condition usually affecting both arms.

Postural tremor: worse when arms stretched out
Improved by alcohol and rest
Most common cause of titubation (head tremor)
Managed with propanolol, or primidone second line

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11
Q

Define Extradural Haemorrhage with its main cause and epidemiology

A

Cranial bleeding above the dura mater.

Usually caused by trauma to pterion of skull, causing rupture of middle meningeal artery in temporo-parietal region. Can associate with temporal bone fracture.

Usually found in young adults

Blood doesnt cross suture lines

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12
Q

Why can extradural stroke present slowly at first before becoming more severe?

A

If bleeding is slow, symptom onset is slower (lucid interval) before there is a sudden, rapid decline when intracranial pressure increases enough to compress brain

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13
Q

Describe non contrast ct appearance in extradural haemorrhage (3)

A

Biconvex, hyperdense haematoma
Blood doesnt cross suture lines
Shows midline shift (increased pressure can cause cause brain shifting/herniation)

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14
Q

What are the 2 main herniation complications of haemorrhagic stroke?

A

Supratentorial herniation (cerebrum against skull, compressing arteries and causing ischaemic stroke)

Infratentorial herniation (Cerebellum pushed against brainstem, compressing area that controls consciousness, respiration, heart rate)

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15
Q

What is cushings triad and how is it treated?

A

Body’s response to increased intracranial pressure, signifies severe lack of oxygen in brain tissue
- Bradycardia
- Irregular respirations
- Widened pulse pressures (increased systolic, decreased diastolic)

Treated with IV mannitol to reduce ICP

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16
Q

Define Subdural haemorrhage with its main cause and epidemiology

A

Bleeding below dura mater, caused by bridging vein rupture.

Usually occur in elderly/alcoholic patients but can occur in babies (shaken baby syndrome)

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17
Q

causes of bridging vein rupture

A

Brain atrophy; with age. Stretches bridging veins, meaning they stretch over gaps unsupported.
Alcohol abuse: Causes walls of vein to thin
Trauma
Falls
Shaken baby syndrome
Acceleration/deceleration injury

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18
Q

non contrast ct appearance of subdural haemorrhage

A

Bleeding between the dura mater and arachnoid
- Follows contours of brain and crosses suture lines, forming a crescent shape

Acute (hyperdense mass)
Chronic (Hypodense mass)
Acute on Chronic (both)

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19
Q

what gcs requires intubation

A

8 or below

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20
Q

specific surgery in subdural haemorrhage

A

Burrhole washout if haemorrhage small

Craniotomy if large haemorrhage

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21
Q

define subarachnoid haemorrhage with main cause

A

Bleeding below the arachnoid layer, where CSF is located.

Main cause is a ruptured saccular (or Berry) aneurysm, with majority located between anterior communicating artery and anterior cerebral artery

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22
Q

RF for subarachnoid haemorrhage (7)

A

PKD (Associated with berry aneurysm)
Connective tissue disorders (Ehlers-Danlos, Marfans)
Family history
Increasing age
HTN
Smoking
Alcohol

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23
Q

typical presentation of subarachnoid haemorrhage

A

Sudden onset occipital “thunderclap” headache, following strenuous activity, with associated neck stiffness and photophobia. Smaller, “Sentinel” headache may have preceded thunderclap

Black, female, 45-70

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24
Q

signs/symptoms of subarachnoid haemorrhage

A

Thunderclap headache
Meningism (Headache, photophobia + neck stiffness)
Fixed dilated pupil (third nerve palsy - especially in posterior communicating artery rupture)
6th nerve palsy
Kernigs and Brudzinskis due to meningism also
Nausea/vomiting, weakness, confusion, coma, reduced consciousness, speech reduction

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25
Q

ix of subarachnoid haemorrhage

A

Urgent non contrast CT head (blood in subarachnoid space/basal cisterns)
CT angiography to locate bleed source
ECG to detect arrhythmia/abnormality

If CT non conclusive,
- Lumbar puncture (RBCs in CSF and Xanthochromia) 12 hours after onset.

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26
Q

Define Kernig’s and Brudzinski’s signs

A

Kernig - Inability to straighten bent leg without pain when hip flexed to 90 degrees

Brudzinski - Passive flexion of neck in supine patient elicits hip and knee flexion

Suggest meningitis/meningism

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27
Q

ct appearance in subarachnoid haemorrhage

A

Blood in subarachnoid space (hyperdense)
- Star shaped lesion (Blood filling in gyro pattern)

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28
Q

Mx of subarachnoid haemorrhage

A

Surgical 1st/GOLD
- Endovascular coiling (clipping also possible but more complications)

Nimodipine to prevent vasopasms
IV Mannitol to reduce ICP
Sodium valproate for seizures

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29
Q

Define meningitis

A

Inflammation of the meninges (specifically leptomeninges - pia and arachnoid). Can be due to viral, bacterial or fungal cause.

Notifiable disease

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30
Q

Viral Causes of meningitis

A

More common but less severe
- Coxsackie virus
- HSV (Herpes simplex virus)
- Varicella Zoster virus
- Mumps

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31
Q

bacterial causes of meningitis

A

Most common - S. pneumoniae and N. meningitidis

Children - ^ and H influenzae

Elderly and pregnant - Listeria Monocytogenes (pregnant avoid cheese)

Newborns - ^ and Group B strep

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32
Q

How do n meningitidis, s pneumoniae, group b strep and listeria monocytogenes present on gram film?

A

N meningitidis - Gram negative diplococci (Only one that causes non blanching rash!)
S pneumoniae/Group B strep - Gram positive cocci in chains
Listeria monocytogenes - Gram positive bacillus

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33
Q

signs/symptoms of meningitis

A

Signs
- Neck stiffness, headache, photophobia (avoids light)
- Phonophobia (avoid sound)
- Papilloedema (optic disk swelling)
- Kernig sign
- Brudzinski sign
- Non blanching rash (N meningitidis only)

Pyrexia, reduced GCS

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34
Q

ix of meningitis

A

Blood culture 1st line - Bacterial or negative for viral

Lumbar puncture GOLD

Bacterial
- Cloudy/yellow
- Protein high
- Glucose low (<50% normal)
- WCC high (Neutrophil)

Viral
- Clear appearance
- Protein small raise/normal
- Glucose normal (>60% normal)
- WCC high (lymphocytes)

(Gram stain identifies bacteria and CSF PCR identifies viruses)

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35
Q

fungal appearance of csf in meningitis

A

Cloudy and fibrous
Protein high
Glucose low
WCC high - Lymphocytes!

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36
Q

mx of bacterial meningitis

A

Primary care: Immediate IV or IM benzylpenicillin (if suspected meningococcal) and hospital referral

Hospital
- Dexamethasone (steroid)
- Cefotaxime or Ceftriaxone IV

Give Amoxicillin if under 3 months or over 50 to cover listeria
Contact tracing and single dose oral ciprofloxacin for contacts

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37
Q

comps of meningitis

A

Hearing loss
Seizures
Cognitive impairment
Hydrocephalus
Sepsis

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38
Q

Upper motor neurone lesion signs vs lower motor neurone lesion signs

Type of paralysis
-reflexia
Fasciculations
Babinski sign
Voluntary movement
Muscle tone and power

A

UMN
Spastic paralysis
Hyperreflexia
No fasciculations
Babinski positive
Voluntary movement slowed
Muscle tone and power kept

LMN
Flaccid paralysis
Hyporeflexia
Fasciculations
Babinski negative
Voluntary movement gone
Muscle tone and power lost

(babinski - toes curl up when bottom of foot is stroked
fasiculations - brief spontaneous contractions under skin)

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39
Q

define ms

A

Type 4 hypersensitivity reaction in which there is autoimmune attack against oligodendrocytes (which create myelin) in the CNS (Brain/Spinal cord). Causes plaques of demyelination.

Lesions vary, meaning plaques are “disseminated in space and time” - affect different areas of CNS at different times/ events.

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40
Q

disease progression in ms

A

Relapsing remitting (most common) - Episodic flare ups without full recovery in between, meaning flares worsen over time. (Most common and often progress to secondary progressive)
Secondary progressive - Symptoms start getting worse without remission
Primary progressive - Symptoms worsen without remission (/)
Progressive relapsing - Constant attack with superimposed flare ups

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41
Q

what is uhtoffs phenomenon?

A

Symptoms worsen with heat (e.g. hot bath) or exercise.

New myelin is inefficient, and doesn’t tolerate temperature rise effectively.

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42
Q

what triad is associated with ms?

A

Charcot’s neurological triad
- Nystagmus (involuntary side-to-side/up-down rapid eye movements)
- Dysarthria (slowed, slurred speech)
- Intention tremor

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43
Q

signs/symptoms of ms

A

Optic neuritis usually first (Loss of vision, eye pain, pale optic disk, double vision)
Internuclear ophthalmoplegia (eye muscle paralysis which impairs lateral gaze)
Lhermitte’s sign - Electric shock sensation when flexing neck
UPPER motor neurone signs
Bowel, bladder, erectile dysfunction
Ataxia
Sensation loss
(Uhthoff’s and Charcot’s neurological triad already mentioned)

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44
Q

what criteria is used in diagnosis of ms?

A

McDonald criteria (think McDonald’s M!)
- 2 or more relapses with evidence of 2 or more lesions, or one lesion with reasonable history of relapse

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45
Q

ix in ms (3)

A

MRI Brain/Spine
- Demyelinating plaques (new enhance with contrast, old don’t - showing dissemination in space and time)

Lumbar puncture
- Oligoclonal IgG bands in CSF

Visual evoked potential studies (responses to visual stimulus)
- Shows delayed nerve conduction

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46
Q

mx of ms

A

During acute relapse
- Oral/IV methylprednisolone first, cladribine
- Plasma exchange

Maintenance
- Interferon beta
- IV monoclonal antibodies

Cladribine second line in ongoing secondary progressive but causes cancer and is teratogenic

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47
Q

comps of ms and there managements (3)

A

Spasticity - Baclofen and gabapentin
Neuropathic pain/depression - amitriptyline
Physiotherapy for Spasticity and mobility impairment

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48
Q

what are some disease modifying durgs in ms with their indications?

A

relapsing-remitting disease + 2 relapses in past 2 years + able to walk 100m unaided
secondary progressive disease + 2 relapses in past 2 years + able to walk 10m (aided or unaided)
IV Natalizumab - monoclonal antibody
IV Ocrelizumab
Oral fingolimod
SC beta interferon
SC Glatiramer acetate

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49
Q

what is huntingtons?

A

Autosomal dominant trinucleotide repeat disorder, which causes deterioration of nervous system and an excess of dopamine.

Also known as Huntington’s chorea (Chorea= involuntary jerky movements)

HTT gene on chromosome 4 - Mutated Huntingtin proteins aggregate in neuronal cells of caudate and putamen. Causes cell death of GABAergic and cholinergic neruones, causing ACh and GABA deficiency, so less dopamine inhibition. Excess dopamine causes excess movement.

Genetic anticipation - The more copies of the protein DNA polymerase adds on in the sperm, the earlier onset and more severe the disease

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50
Q

signs and symptoms of huntingtons?

A

Usually asymptomatic until 30-50 years
Prodromal - Irritability, depression, cognitive problems
Chorea - Jerky involuntary movements
Eye movement disorders
Dysphagia/dysarthria

Dementia, seizures, death within 15 years

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51
Q

ix in huntingtons

A

Clinical diagnosis
- Genetic testing GOLD

                                                                                                                                                                                                                                                    CT/MRI - Caudate and striatal atrophy - increased size of lateral ventricles
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52
Q

other causes of chorea

A

Hyperthyroid
Wilson’s
SLE
Dementia

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53
Q

mx of huntingtons

A

Uncurable

Chorea
- Diazepam and tetrabenazine (Benzodiazepine and dopamine depleting agent)

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54
Q

define parkinsons disease

A

Neurodegenerative movement disorder characterised by loss of dopaminergic neurones in Substantia Nigra Pars Compacta of basal ganglia.

Misfolded a synuclein proteins called Lewy bodies also present histologically (dark eosinophilic inclusions)

Causes a dopamine deficiency

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55
Q

what are the parkinsonism symptoms

A

Resting Tremor
Bradykinesia
Rigidity
Postural instability

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56
Q

signs and symptoms of parkinsons (other than parkinsonisms)

A

Resting tremor
Cogwheel rigidity
Shuffling gait
Reduced arm swing

Non motor:
Loss of smell
Sleep disturbance
Depression, anxiety
Dementia

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57
Q

ix in parkinsons

A

Clinical diagnosis - bradykinesia and 1 other Parkinsonism sign
(Bradykinesia = slow, difficult movements. Smaller handwriting, shuffling gait, reduced arm swing etc)

Dopamine agent trial shows improvement

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58
Q

mx of parkinsons

A

If Severe: Levodopa + Decarboxylase inhibitor (boost dopamine and Di prevents L-dopa breakdown)
- Co-careldopa (Levodopa and carbidopa)

Otherwise:
Dopamine agonist
- Ropinirole

Monoamine oxidase B inhibitor (MAOBi) (stop breakdown of circulating dopamine)
- Selegiline

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59
Q

comps of parkinsons

A

Disease progression and motor fluctuations (off periods when treatment stops working)
- Freezing (sudden stop of movement)
- Dyskinesia
- Dementia

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60
Q

differentials of parkinsonisms

A

Benign Essential Tremor
Wilson’s disease
Encephalitis causing degeneration of substantia nigra
Trauma

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61
Q

define myasthenia gravis

A

Type 2 hypersensitivity reaction causing autoimmune destruction of the post synaptic membrane at the neuromuscular junction of skeletal muscle. Antibodies to acetylcholine receptors in 85% of cases. (Anti-AChR)

2x in women.

Mostly affects facial muscles.

Strong association with thymoma/ thymic hyperplasia

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62
Q

signs/symptoms of myasthenia gravis (6)

A

Mostly affects proximal and small muscles of head and neck
- Muscle weakness with fatigability, worse with exertion better with rest (e.g. patient counting to 50 will struggle in later numbers)
- Ptosis (eyelid droop) and diplopia (double vision)
- Jaw weakness and weak swallow (dysphagia)
- Head drop
- Facial paresis and slurred speech
- Snarl when attempting to smile (myasthenic snarl)

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63
Q

how to check for muscle fatigability on examination (3) and what should you check? (myasthenia)

A

Repeated blinking causing ptosis
Counting to 50, speech becomes slurred and quieter towards end
Repeated abduction of one arm will result in weakness in said arm compared to other

Forced Vital Capacity should also be checked

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64
Q

ix in myasthenia gravis?

A

Antibodies
- AchR antibodies (anti-MuSK and anti-LRP4 less sensitive)
- Anti-MUSK
- Anti LRP4

CT thorax - look for thymus growth/thymoma (rule out)

Tensilon test - Used to be done but causes arrhythmia so dont even think about it

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65
Q

drugs that exacerbate MG muscle fatigability

A

penicillamine
quinidine, procainamide
beta-blockers
lithium
phenytoin
antibiotics: gentamicin, macrolides, quinolones, tetracyclines

Most common factor is exertion!

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66
Q

mx of myasthenia gravis

A

Long acting acetylcholinesterase inhibitor
- Pyridostigmine first line

Immunosuppression (not started at diagnosis, usually started later)
- Prednisolone

Thymectomy may be needed (as many patients also have thymic hyperplasia)

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67
Q

myasthenia gravis brief pathophysiology

A

Unexplained destruction of Only UMNs and LMNs.
- No effect on sensory neurones (distinguishing point from MS etc)
- No effect on eyes (distinguishing from myasthenia gravis)
- No cerebellar involvement
- SOD1 mutation association in ALS

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68
Q

Define guillain barre syndrome with causes

A

Acute autoimmune demyelination of the peripheral nervous system, following an upper resp tract or GI infection (e.g. gastroenteritis)

Acute, symmetrical, ascending weakness!

Can be caused by:
Bacteria:
- Campylobacter Jejuni
- M. pneumoniae

Viral:
- Cytomegalovirus
- EBV

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69
Q

guillaine barre disease course (4)

A

Initial GI or URT infection
Symptoms start after 2 weeks
Symptoms peak 2-4 weeks further
Recovery period of months to years

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70
Q

pathophysiology of guillain barre syndrome

A

Molecular mimicry.

Pathogenic antigens resemble Schwan cell proteins so when immune response is launched, there is also destruction of myelin sheath. Demyelination occurs in patches down length of axon (segmental demyelination). Schwann cells can remyelinate so patients recover over time. Affects sensory and motor nerves.

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71
Q

signs and symptoms of guillain barre syndrome

A

Symptom onset 2-3 weeks after preceding infection. Proximal muscles affected first

Symmetrical ascending weakness beginning in legs/feet.

Areflexia
Reduced sensation
Paraesthesia
Sensory loss
Respiratory distress if lungs affected
Autonomic dysfunction (bowel/bladder, sweating, raised BP/pulse, arrhythmia)

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72
Q

ix of guillain barre syndrome

A

Brighton criteria used to make clinical diagnosis, can be supported by:
- Nerve conduction studies (reduced conduction)
- Lumbar puncture (high protein in CSF, normal cell count and glucose)

Antibodies: subtype of GBS
AIDP (90%) - Anti ganglioside
Miller fisher syndrome (eyes affected first) - anti GQ1b

Do spirometry to assess risk of resp failure

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73
Q

mx of guillain barre syndrome (2 tx + 2 complication tx)

A

IV immunoglobulin 5 days (CI if IgA deficiency)
Plasma exchange

VTE Prophylaxis (LMWH)
Ventilation if low FVC

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74
Q

umn lesion area

A

anywhere from pre central gyrus to anterior spinal cord

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75
Q

lmn lesion area

A

anwhere from anterior spinal cord to innervated muscle

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76
Q

how is muscle power affected in umn lesions?

A

In arms flexors>extensors
In legs extensors>flexors

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77
Q

types of mnd

A

Amyotrophic lateral sclerosis (50% of patients)
typically LMN signs in arms and UMN signs in legs
in familial cases the gene responsible lies on chromosome 21 and codes for superoxide dismutase

Primary lateral sclerosis
UMN signs only

Progressive muscular atrophy
LMN signs only
affects distal muscles before proximal
carries best prognosis

Progressive bulbar palsy
palsy of the tongue, muscles of chewing/swallowing and facial muscles due to loss of function of brainstem motor nuclei
carries worst prognosis

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78
Q

presentation of mnd

A

asymmetric limb weakness is the most common presentation of ALS
the mixture of lower motor neuron and upper motor neuron signs
wasting of the small hand muscles/tibialis anterior is common
fasciculations
the absence of sensory signs/symptoms
vague sensory symptoms may occur early in the disease (e.g. limb pain) but ‘never’ sensory

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79
Q

mx of mnd (2)
what is prognosis?

A

Riluzole (protects neurones from glutamate induced damage)
Respiratory support (non invasive at home)

50% die in 3 years

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80
Q

gene associations with alzheimers?

A

APoE e4 - APoE usually helps break down beta amyloid but e4 version less effective.
Down’s (Trisomy 21) - Increased APP (amyloid precursor protein) production (APP gene also on C21). APP broken down incorrectly becomes beta amyloid.
PSEN1, PSEN2

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81
Q

key histological findings in alzheimers

A

Senile plaques of beta amyloid proteins (APP incorrectly broken down into sticky, insoluble b amyloid) (extracellular)

Neurofibrillary tangles of hyperphosphorylated tau proteins (intracellular)

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82
Q

signs/symptoms of alzheimers (4)

A

Insidious onset and slow progressive decline

Poor memory (short term early, long term late)
Speech problems (receptive and expressive dysphagia)
Loss of executive function (planning/problem solving)
Disorientation/lack of recognition of places, people or objects

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83
Q

how would alzheimers affect behaviour? (4)

A

Emotional instability
Depression/anxiety
Withdrawal/apathy
Disinhibition (Socially/sexually inappropriate behaviour)

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84
Q

how would alzheimers affect daily living? (3)

A

Loss of independence
Early on loss of higher level function (finances, difficulties working)
Later loss of basic function (washing, eating, walking)

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85
Q

how is alzheimers diagnosed?

A

Based on DSM-V criteria and MMSE (Mini mental state examination) (25+ normal, <17 severely impaired)

MRI - Generalised brain atrophy with medial temporal then later parietal predominance

Brain biopsy is GOLD but can only be done after death

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86
Q

Mx of alzheimers

A

Supportive: Improve cognitive function
- Exercise
- Music
- Board games
- Cognitive stimulation program

ACh-esterase inhibitor (Donepezil)
NMDA receptor antagonist (Memantine)

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87
Q

Define Vascular dementia

A

Dementia caused by cerebrovascular damage causing hypoperfusion of neuronal cells.

Presents in patients with Stroke/TIA history, UMN signs and general condition decline.

Shows a stepwise decline with symptoms worsening after each cerebrovascular event.

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88
Q

Investigations and treatment of vascular dementia

A

Mini mental state exam

CT/MRI of brain
- Multiple cortical and subcortical infarcts
- Atrophy of brain cortex

Treated with management of risk factors (lower BP, cholesterol, diabetes etc)

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89
Q

define lewy body dementia

A

Dementia with Parkinsonism (Resting tremor, bradykinesia, rigidity, postural instability).

Alpha synuclein misfolds in neurones and aggregates to form Lewy Bodies, which deposit in cortex and substantia nigra causing neuron death.

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90
Q

sx of lewy body dementia

A

Presents with dementia symptoms first
(memory, focus, speech, understanding issues)

Parkinsonism develops later

Sleep disorders like sleep walking/talking, and hallucinations are also very common in LBD

If Parkinsons first, it is Parkinson Dementia

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91
Q

mx of lewy body dementia

A

Dopamine analogue - Levodopa
ACh-esterase inhibitor - Donepezil

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92
Q

Define fronto temporal dementia

A

Focal degeneration of frontal and temporal lobes. Pick’s disease is most common type. Loss of over 70% of spindle neurones.

Frontotemporal dementia (Pick’s disease)
Progressive non fluent aphasia (Chronic progressive aphasia)
Semantic dementia

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93
Q

common features of frontotemporal lobar dementias

A

Onset before 65
Insidious onset
Relatively preserved memory and visuospatial skills

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94
Q

What is Pick’s disease, how does it present and what macroscopic and microscopic changes are found

A

AKA Frontotemporal dementia.

Personality change and impaired social conduct! Hyperorality, disinhibition, increased appetite, perserveration beahviours.

Focal gyral atrophy with knife-blade appearance

Macro
- Atrophy of frontal and temporal lobes

Micro
- Pick bodies - spherical aggregations of tau protein (silver staining)
- Gliosis
- Senile plaques and neurofibrillary tangles

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95
Q

What is cpa? (chronic progressive aphasia?

A

Clues in the name.

Short utterances that are agrammatic. Comprehension preserved

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96
Q

what is semantic dementia?

A

Fluent progressive aphasia. Speech fluent but empty, not much meaning. Memory better for recent rather than remote events

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97
Q

what are pick bodies?

A

3R isoform of tau proteins

These become hyperphosphorylated and form tangles, causing atrophy in frontoteporal lobes

(In alzheimers, the isoform is 3R+4R)

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98
Q

Give primary and secondary causes of headache

A

Primary
- Migraine
- Tension
- Cluster

Secondary (to other pathology)
- GCA
- Cerebrovascular disease
- Subarachnoid haemorrhage
- Truma

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99
Q

define migraine

A

Episodes of recurrent, unilateral throbbing headache. May or may not have an aura and often has visual changes (e.g. photophobia, diplopia etc).

Can last up to 72 hours, and classically preceded by an aura
- Visual, progressive, lasting 5-60 minutes.

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100
Q

Common migraine triggers

A

CHOCOLATE
Chocolate
Hangover
Orgasms
Cheese
Oral contraceptive
Lie ins (tiredness)
Alcohol
Tumult (loud noise)
Exercise

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101
Q

Signs/symptoms of typical/atypical aura

A

Typical: Lasts 5-60 mins and fully reversible.
- Visual changes (zigzag lines, distortion etc)
- Smell changes
- Paraesthesia

Atypical: >60 mins
- Diplopia
- Motor weakness (hemiplegic migraine!)
- Poor balance
- Reduced consciousness

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102
Q

Ix in migraine

A

Clinical diagnosis:

Migraine with/without aura
(at least 2/4 symptoms, 1 associated symptom, no attribution to another disorder)

CT/MRI to exclude secondary haemorrhage
ESR exclude GCA

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103
Q

tx of migraine

A

Acute prevention
- Oral Sumatriptan (5-HT receptor agonist (mimic serotonin))
with/without aspirin

Prophylaxis
- Propanolol
- Amitriptyline
- Topirimate (antiemetic)

AVOID Opiates

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104
Q

define tension headache

A

Most common type of headache.
Bilateral “pressing/tight” headache. Lasts minutes to hours. No associated symptoms except photo OR phonophobia

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105
Q

Define cluster headache

A

Severe, unilateral periorbital headache, with associated autonomic features, affecting same side face/eyes. Lasts 15-180 mins.

AKA Trigeminal Autonomic Cephalalgia

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106
Q

Signs/symptoms of cluster headache

A

Severe unilateral, periorbital, crescendo headache, lasting 15mins to 3 hours. Clusters of headaches,
(Boring/hot poker pain “worst pain ever”)

Ipsilateral autonomic symptoms
- Ptosis (eyelid droop)
- Miosis (excessive constriction of pupil of eye)
- Teary, bloodshot eye
- Nasal congestion/rhinorrhoea

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107
Q

diagnosis and mx of cluster headache

A

Clinical diagnosis (5+ similar headaches)

Acute
- Triptans
- High flow oxygen
(AVOID paracetamol, NSAID, Opioids)

Prophylaxis
- Verapamil (CCB)
- Prednisolone, 2-3 weeks

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108
Q

define trigeminal neuralgia

A

Severe, unilateral “electric” pain along distribution of trigeminal nerve lines. Extremely increased risk in demyelinating disease. Attacks last seconds.

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109
Q

Pathophysiology of trigeminal neuralgia

A

Vascular loop (MC superior cerebellar artery) compresses nerve near nerve root entry zone. Compression causes poor conduction along nerve root, causing pain.

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110
Q

common triggers of trigeminal neuralgia pain

A

Light touch (washing, shaving, brushing teeth)
- Talking
- Cold weather
- Spicy food
- Caffeine and citrus

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111
Q

What are the branches of the trigeminal nerve

A

Ophthalmic
Maxillary
Mandibular

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112
Q

Signs/Symptoms of trigeminal neuralgia?

A

Facial pain
- Electric/stabbing pain
- Very severe
- Trigeminal distribution
- Unilateral
- Provoked (touch, cold etc)

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113
Q

Ix and Mx of trigeminal neuralgia

A

Clinical but can MRI brain (space occupying lesion, demyelination etc)

Carbamazepine first line
Surgery (microvascular decompression)

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114
Q

define cauda equina

A

Compression of the bundle of nerves below the end of the spinal cord (known as cauda equina). Causes bilateral lower limb weakness/saddle anaesthesia

Medical emergency that requires immediate decompression

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115
Q

Signs/Symptoms of cauda equina

A

Severe lower back pain, bilateral lower limb weakness and reduced sensation. LMN signs!

Saddle anaesthesia (numbness/reduced tone in perianal region, groin, inner thigh)
Decreased reflexes and leg weakness/paralysis
Erectile dysfunction
Bladder/bowel dysfunction.

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116
Q

Ix and tx of cauda equina

A

URGENT MRI spine GOLD

Emergency decompressive laminectomy (vertebra removal) within 24-48 hours, or permanent weakness/dysfunction

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117
Q

brief overview of anatomy of spine

A

Originates at base of medulla oblongata, exiting through foramen magnum, ending at conus medullaris at L2

Consists of 5 sections of vertebrae, with 31 spinal nerves arising from this
- Cervical (7)
- Thoracic (12)
- Lumbar (5)
(Spinal cord ends at L1, conus medullaris begins at L2)
- Sacrum (5 - fused)
- Coccyx (4 - fused)

Beyond L2 are bundle of nerves called “cauda equina”

118
Q

causes of spinal cord compression

A

Vertebral body neoplasms (thoracic most likely)
- disc herniation
- disc prolapse
- infection
- Trauma
- Spinal stenosis

119
Q

how do spinal cord lesions secondary and motor symptoms present?

A

Motor - Contralaterally
Sensory - Ipsilaterally (same side)

120
Q

what nerve roots are implicated in knee jerk, big toe jerk and ankle jerk reflexes?

A

Knee jerk - L3/4
Big toe - L5
Ankle - S1

121
Q

signs/symptoms of spinal cord compression

A

Progressive (Hours-weeks/months) back pain and progressive leg weakness. Motor signs contralateral

UMN signs above level of lesion
LMN below level of lesion
Sensory loss 1-2 cord segments below lesion level
bladder/sphincter involvement is a late, bad signs

122
Q

what levels are lesions in l5 nerve root compression and sciatica?

A

L5 nerve root compression - L4/L5

Sciatica - L5/S1

123
Q

specific causes of peripheral neuropathy

A

DAVID

Diabetes
Alcoholism
Vitamin B12 deficiency
Infective/inherited (GBS/Charcot-Marie-Tooth)
Drugs e.g. isonazid

124
Q

what is brown sequard syndrome?

A

Damage to one half of the spinal cord, resulting in a specific pattern of symptoms:
- Ipsilateral motor weakness

Ipsilateral loss of proprioception (position sense), light touch, vibration at level of lesion
Contralateral loss of pain and temperature sense below level of lesion

125
Q

gold ix and mx of brown sequard

A

Investigations
- EMG (electromyography)
- MRI Spinal cord

Management
- Treatment of underlying condition
- High dose steroids

126
Q

Define/ explain pathophysiology of Charcot Marie Tooth syndrome

A

Group of inherited diseases (autosomal dominant) that cause axonal/myelin dysfunction. CMT1 and CMT2 most common

CMT 1 - loss of myelin sheath (onion bulb myelin due to schwann cell repair)
CMT 2 - Neuronal mitochondrial dysfunction = neurone death

Causes atrophy of muscle when motor neurones affected

127
Q

Signs/symptoms of charcot marie tooth

A

Weakness in lower legs and hands.
Loss of muscle tone and reflexes
Foot drop and claw hand
Tingling/burning in hands and feet
Thickened palpable nerves and hammer toes
“Inverted champagne bottle” legs due to distal muscle wasting

128
Q

Define Duchenne Muscular Dystrophy

A

X linked recessive condition characterised by severe muscle dystrophy due to absence of Dystrophin protein

129
Q

Signs/symptoms of duchenne muscular dystrophy

A

Usually presents 3-5 years.
- Weakness in pelvic muscles
- Waddling gait
- Gowers sign: due to inability to get up normally, they get into downward dog position then climb their hands up their legs to stand.
- Fat calves due to buildup of fat and fibrotic tissue rather than muscle

130
Q

Nerves implicated in wrist drop and claw hand

A

WD - Radial
Cl - Ulnar (4th and 5th fingers claw)

131
Q

What is Bells palsy

A

Acute, unilateral, idiopathic facial nerve paralysis.

Aetiology unknown, but suspected HSV

132
Q

How does Bells palsy present

A

LMN Facial nerve palsy -> Forehead affected
(UMN spares upper face)
- Post auricular pain
- Altered taste
- Dry eyes
- Hyperacusis

133
Q

How is Bell’s palsy treated

A

Prednisolone within 72 hours, maybe add antiviral

most people with Bell’s palsy make a full recovery within 3-4 months

134
Q

What is temporal arteritis

A

AKA Giant cell arteritis. Branches of carotid artery (

Occurs in >50, usually ~70. Strong association with Polymyalgia Rheumatica.

Early recognition and treatment can minimise risk of complications e.g. permanent sight loss.

135
Q

How does temporal arteritis present

A

Rapid <1 month onset
Unilateral headache around temple/forehead
Diminished/absent temporal artery
Jaw claudication
Blurred/double vision
Optic disc pallor
Scalp tenderness (Painful to comb)
Fever, muscle aches, weight loss, loss of appetite

136
Q

GCA typical presentation

A

50+ white female with unilateral temple headache, scalp tenderness (painful to comb), jaw claudication and vision changes.

137
Q

Pathophys of GCA

A

Granulomatous vasculitis of large/medium arteries. Arteries become inflamed, intima is thickened and vascular lumen is narrowed. Usually cerebral (temporal) arteries affected:
- Superficial temporal artery: Headache/scalp tenderness
- Mandibular artery: jaw claudication
- Ophthalmic artery: visual loss (retinal ischaemia)

138
Q

Diagnostic criteria in GCA

A

3 of:
- Over 50
- New headache
- Temporal artery tenderness/diminished pulse
- ESR Raised
- Abnormal temporal artery biopsy

139
Q

Management of GCA

A

High dose prednisolone

Sight loss (amaurosis fugax!)
Should be dealt with ASAP or could lead to permanent blindness
Ischaemic cranial complications (Visual loss/stroke)
Aortic aneurysm

140
Q

In cases where long term steroids are given, what 2 systems should be protected and how is this done?
GCA

A

GI (stomach and oesophagus) and Bones
- PPI (omeprazole)
- Alendronate (bisphosphonate)
- Ca2+ and vitamin D

141
Q

Define Polymyalgia Rheumatica

symptoms

ix

mx

A

Condition that causes pain stiffness and inflammation in neck, shoulders and hips. Limits range of motion. Occurs alongside GCA often.

Morning pain/stiffness in shoulders etc. Leads to fatigue, fever, weight loss, anorexia and depression

Raised ESR but CK and EMG normal

Managed with prednisolone

142
Q

What is Broca’s area, and what does an injury of it cause?

A

Located in the frontal lobe of person’s dominant side (left in right handed people) and influences motor production of speech.

Causes expressive aphasia - Patients can understand speech but can’t produce it themselves

143
Q

What is Wernickes area and what does injury of it cause

A

Located in parietal and temporal lobe of person’s dominant side (left in right handed people) , influences understanding of speech and using correct words to express thoughts

Causes receptive aphasia - Patients can produce speech but don’t understand the meaning of spoken words

144
Q

What are Wernickes and Brocas areas supplied by?

A

Middle Cerebral Artery

145
Q

What is a watershed area?

A

Areas furthest from blood supply, most susceptible to infarction

146
Q

Define ischaemic stroke

A

Reduced cerebral blood flow due to arterial occlusion or stenosis. Account for 85% of all strokes.

Consists of rapidly developing signs of cerebral dysfunction, lasting more than 24 hours, with no apparent cause.

147
Q

Causes of ischaemic stroke

A

Disruption of blood supply secondary to:
- Thrombus formation/ embolus
- Atherosclerosis
- Shock
- Vasculitis
- Hypercoagulability (thrombophilia)

148
Q

Risk factors for stroke (9)

A

Male
Old (>55)
Black or Asian
History of Ischaemic stroke or TIA
Atrial fibrillation
Sickle cell disease
Combined contraceptive pill
Carotid artery stenosis
Smoking, obesity, HTN, T2DM

149
Q

Define hemiparesis

A

Weakness or paralysis on one side of the body

150
Q

Manifestations of an Anterior Cerebral Artery ischaemic stroke

A

Contralateral hemiparesis and sensory loss, affecting lower limbs>upper limbs

151
Q

Manifestations of middle cerebral artery stroke

A

Contralateral hemiparesis and sensory loss affecting upper limbs>lower limbs.
Aphasia if affecting Broca or Wernickes areas in dominant hemisphere
Homonymous hemianopia (visual field defect in same side of both eyes)

152
Q

Manifestations of Posterior Cerebral Artery stroke

A

Contralateral homonymous hemianopia with macular sparing (preservation of central visual field)
Contralateral loss of pain and temperature

153
Q

Manifestations of Vertebrobasilar artery stroke

A

Cerebellar signs (intention tremor, nystagmus, hypotonia)
Reduced consciousness
Quadriplegia

154
Q

Manifestations of Webers syndrome (midbrain infarct)

A

Oculomotor palsy and contralateral hemiplegia

155
Q

Manifestations of Lateral medullary syndrome (posterior inferior cerebellar artery occlusion)

A

Ipsilateral facial loss of pain and temperature
Ipsilateral Horner’s syndrome: miosis, ptosis, anhidrosis
Ipsilateral cerebellar signs
Contralateral loss of pain and temperature

156
Q

What is lacunar stroke?

A

Stroke affecting small branches of middle cerebral artery.

Causes one of the following:
Pure motor loss
pure sensory loss,
ataxic hemiparesis

157
Q

What is pronator drift

A

Ask patient to raise arms. On the affected side, palm and arm will face inward and downwards. Suggests muscle weakness.

(Symptoms contralateral to affected brain side)

158
Q

What assessment system is used in acute strokes

A

ROSIER (Recognition of Stroke In Emergency Room)

Uses symptoms as + points and mimics (syncope, seizure activity) as - points

159
Q

Investigations on stroke presentation

A

Assessment using ROSIER scale
(stroke possible if >0)
Non contrast CT head (rule out haemorrhagic stroke)
CT Angiogram (identify occlusion - hypoattenuation of brain parenchyma, loss of matter differentiation)

160
Q

How do strokes appear on CT

A

Ischaemic - Darkness of brain parenchyma
Haemorrhagic - Brightness surrounded by darkness (blood surrounded by oedema)

161
Q

Management of ischaemic stroke

A

Once haemorrhagic ruled out:
- IV Alteplase if presents within 4.5 hours
- Mechanical thrombectomy if after 4.5 hours

Then: 300mg Oral aspirin daily for 2 weeks then clopidogrel lifelong daily

162
Q

What are the driving rules in ischaemic stroke

A

Patients must not drive car for 1 month after TIA or stroke, or 1 year for HGV

163
Q

What classification system is used in stroke?

A

Bamford classification - categorises stroke based on area of circulation affected.

Total anterior circulation stroke - Anterior/middle cerebral artery (all 3 - Unilateral weakness of face,arm or leg, homonymous hemianopia, higher cerebral dysfunction)
Partial anterior circulation stroke - only part of anterior circulation (2 out of 3 symptoms)
Lacunar - Either: All sensory, all motor or ataxic hemiparesis
Posterior circulation syndrome (1 of cranial nerve palsy, bilateral motor/sensory defecit, eye movement disorder, homonymous hemianopia)

164
Q

Scoring system for risk of stroke after Atrial Fibrillation

A

CHA2DS2 VASc

165
Q

DEFINE TIA

A

Transient Ischaemic Attack. Acute neurological dysfunction that has a sudden onset and resolves in less than 24 hours.

NOT a stroke as involves ischaemia not infarction

166
Q

Symptoms of TIA

A

Contralateral numbness, face drooping, dysphasia, vision loss
Amaurosis Fugax
Same as stroke but lasts less than 24 hours and no lasting effects

167
Q

What acronym helps identify stroke in public

A

FAST
Face
Arms
Speech
Time

168
Q

Define amaurosis fugax with pathophysiology and causes

A

Short lived blindness in one eye described as “curtain coming down over vision”. Due to temporary reduction in internal carotid or central retinal artery leading to ischaemia of the retina.

Occurs in GCA, Stroke, AF

169
Q

What risk score should be completed after TIA

A

ABCD2 - risk of stroke after TIA
Age >60
BP >140/90
Clinical features (unilateral weakness =2, just speech disturbance =1)
Duration >60mins =2, 10-59mins =1

> 6 predicts stroke, immediate referral
4 requires referral

170
Q

MX OF TIA

A

1st line - 300mg Aspirin daily for 2 weeks
- Clopidogrel daily long term
- Atorvastatin

ABCD2 score to assess stroke risk

171
Q

What is it called when 2 TIAs happen in close proximity

A

Crescendo TIAs.
Requires urgent referral

172
Q

What are the layers over the brain called

A

Meninges of the brain

Dura mater
Arachnoid
Pia mater (innermost layer)

173
Q

What are the types of haemorrhagic stroke

A

Extradural haemorrhage - bleeding above dura mater

Sudural haemorrhage - bleeding between dura and arachnoid

Subarachnoid haemorrhage - bleeding between arachnoid and pia mater

Intracerebral haemorrhage - Bleeding within cerebrum

174
Q

Risk factors for haemorrhagic stroke (6)

A

Head injury
Hypertension
Aneurysms
Brain tumour
Connective tissue disorder
Family history

175
Q

General symptoms of haemorrhagic stroke

A

Reduced GCS
Headache
Vomiting
Seizures
One sided arm/leg/face weakness/paralysis

176
Q

Give the scoring system for unconsciousness

A

Glasgow Coma Scale - assessment of eye opening, verbal and motor response.

Minimum score 1 per category

177
Q

Give the scoring system for consciousness

A

Glasgow Coma Scale - assessment of eye opening, verbal and motor response.

Eye out of 4
Verbal out of 5
Motor out of 6

Minimum score 1 per category

178
Q

Glasgow coma scale scoring system in detail (not sure if need to know but probably helpful to have decent idea)

A

Eye opening
4 - Spontaneous
3 - To speech
2 - To pain
1 - None

Verbal response
5 - Orientated
4 - Confused conversation
3 - Inappropriate words
2 - Incomprehensible sounds
1 - None

Motor response
6 - Obeys command
5 - Localises to pain
4 - Withdraws to pain
3 - Abnormal flexion to pain
2 - Extension of upper and lower limbs to pain
1 - No response

179
Q

why might someone get a brain abscess?

A

extension of sepsis from middle ear or sinuses

trauma or surgery to scalp

penetrating head injury

embolic event from endocarditis

180
Q

presenting sx of brain abscess

A

depend on site of abscess - if motor cortex will present earlier

mass effect on brain and raised icp

headache: dull persistent
fever: poss absent. not swinging pyrexia though
focal neurology: oculomotor nerve palsy or abducens nerve palsy secondary to raised icp

nausea
papilloedema
seizures

181
Q

how would you investigate for brain abscess

A

ct scanning

182
Q

how would you manage for brain abscess

A

surgery - craniotomy - debride abscess cavity.
abscess can reform because head is closed after abscess drainage

iv abx: 3rd gen cephalosporin+ metronidazole

icp manage: dexamethasone

183
Q

features of encephalitis

A

fever headache psychiatric sx , seizures, vomiting

focal features: aphasia

altered cognition/conciousness. unusual behaviour.

peripheral lesions: like cold sores no relationship to presence of HSV encephalitis

184
Q

pathophysiology of encephalitis

A

hsv-1 - 95% adult cases

affects temporal and inferior frontal lobes

185
Q

ix encephalitis

A

csf - lymphocytosis, elevated protein
pcr: HSV,VSV,ENTEROVIRUSES

neuroimaging:
CT - medial temporal and inferior frontal changes - eg petechial haemorrhages
normal in 1/3 of patients
MRI is better
hiv test
swabs - causative organism, throat and vesicle swab

EEG: lateralised periodic discharges at 2Hz

186
Q

mx encephalitis

A

intravenous aciclovir start in all suspected encephalitis cases - hsv and vsv
ganciclovir - cmv

187
Q

comps of encephalitis

A

lasting fatigue/prolonged recovery
headache, chronic pain, learning disability, change to memory, personality, mood , cognition.

movement disorder
sensory disturbance
siezure
hormonal imbalance

188
Q

ci of lp in encephalitis in kids

A

gcs below 9
haemodynamiccaly unstable
active seizures
post-ictal

189
Q

causes of encephalitis in kids

A

non infective: autoimmune

mc : viral
bacterial and fungal - rare

mc: hsv. hsv-1 from cold sores.
in neonates: hsv-2 from genital herpes from birth.

vzv: chicken pox,cmv associated with immunodeficiency.
ebv: infectious monucleosis, adenovirus, influenza virus.

polio, mumps, rubella, measles - all can cause it too.

190
Q

hsv encephalitis - typically affects with lobes

A

temporal

191
Q

what is shingles herpes zoster?

A

acute unilateral painful blistering rash

caused by reactivation of varicella-zoster virus - vzv.

(following vzv infection, chickenpox)
virus lies dormant in dorsal root or cranial nerve ganglia.

192
Q

risk factors of shingles

A

increasing age
hiv: strong rf 15* more common

other immunosuppressive conoditions: steroids, chemo

193
Q

most common affected dermatomes in shingles

A

t1-l2

194
Q

features of shingles

A

prodromal period:
- burning pain over affected dermatome for 2-3 days.
-pain might be severe and sleep
- 20% pts experience fever, headache, lethargy

rash
- erythematous, macular rash over affected dermatome
-quickly becomes vesicular
- characteristically well demarcated by dermatome dont cross midline. “ bleeding” in adjacent areas might be seen.

clinical diagnosis

195
Q

how would you manage shingles - herpes zoster

A

avoid pregnant women and immunosuppresed - contagious

infectious until vesicles crusted over, 5-7 days after onset. covering lesions reduces risk.

analgesia:
- 1st line para and nsaids
- if not : neuropathic agent like amitriptyline
- oral corticosteroids - in 1st 2 weeks in immunocompetent adults with localised shingles if pain severe.

antivirals
- within 72 hrs for most patients, unless pt under 50 and mild truncal rash with mild pain
- aciclovir , famciclovir, valaciclovir

196
Q

benefit of prescribing antiviral in shingles - herpes zoster

A

reduced incidence of post-herpetic neuralgia

197
Q

complications of shingles -herpes zoster

A

postherpetic neuralgia

herpes zoster opthalmicus - ocular division of trigeminal nerve

herpes zoster oticus - ear lesions and facial paralysis

198
Q

malaria is caused by?

A

plasmodium protozoa spread by female anopheles mosquito:
4 diff :

plasmodium falciparum - most.
plasmodium vivax - 2nd - benign malaria
plasmodium ovale
plasmodium malariae

199
Q

malaria protects from what diseases?

A

sickle-cell trait

g6pd deficiency
hla b53
absence of duffy antigens

200
Q

falciparum malaria - mc - most severe type: features - classic triad

why do they occur every 48 hrs?

A

paroxysms of fever chills and sweating.

every 48 hrs because erythrocytic cycle of plasmodium falciparum parasite.

fever high intermittent. - possible rigors too.

non specific:
malaise,headache,myalgia

201
Q

general features of falciparum malaria

A

fever - cyclical - sweating and sometimes rigors.

gi:
-anorexia,n+v, abdo pain. diarhoea poss , mc in kids. poss mild jaundice and occasional pruritus

resp: cough, poss mild tachypnoea

msk: generalised body aches and joint pain

neuro: headache. dizziness and sleep disturbance.

cv: tachy, hypotension more typical of severe malaria.

haem: thrombocytopenia most significant haematological finding. mild anaemia poss

renal: aki associated with severe malaria. non severe : mild-moderate increase in creatinine or blood urea nitrogen levels

202
Q

features of severe falciparum malaria

how to treat

A

schizonts on blood film

parasitaemia >2%

hypogly
acidosis
temp over 39
severe anaemia

iv artesunate
if parasite count over 10% then exchange tranfusion

shock might show bacterial septicaemia

203
Q

comps of malaria falciparum

A

cerebral malaria: seizures, coma
acute renal failure: blackwater fever, secondary to intravascular haemolysis

ards
hypogly
dic

204
Q

how would you manage falciparum malaria?

A

uncomplicated falciparum:
1st line: artemisinin-based combo therapy (acts) - artemether+ lumefantrine, artesunat+ amodiaquine, artesunate+ mefloquine, artesunate + sulfadoxine-pyrimethamine, dihydroartemisinin + piperaquine

205
Q

mc non falciparum malaria

A

vivax - central america and indian subcontinent.
then ovale (africa) and malariae.

knowlesi - south east asia

206
Q

features of non falciparum malaria

A

fever headache splenomegaly

vivax/ovale: cyclical fever every 48 hrs.
malariae: cyclical fever every 72 hours. associated with nephrotic syndrome.

ovale and vivax: hypozoite stage : relapse after tx.

207
Q

how would you treat non falciparum malaria?

A

artemisinin-based combo therapy (act) or chloroquine
if chloroquine resistant.

act avoid in pregnancy.

ovale/vivax: primaquine after acute tx with chloroquine to destroy liver hypnozoites and prevent relapse

208
Q

incubation period of malaria

A

1-4 weeks after exposure.

vivax and ovale can lie dormant upto 4 yrs

209
Q

how do you diagnose malaria

A

blood film.
edta bottle.

3 negative samples over 3 consecutive days needed to exclude.

210
Q

side effect of primaquine

A

can cause severe haemolysis in g6pd pts

211
Q

doxycline - use in malaria when to give etc

side effedcts

A

broad spect abx

se: diarrhoea , thrush. skin sensitivity to sun

take 2 days before until 4 weeks after endemic area travel.

212
Q

antimalarial meds

A

proguanil with atovaquone
doxycycline
mefloquine - psych side effects. - anxiety,dep,abnormal dreams
chloroquine with proguanil

213
Q

general advice preventing malaria

A

mosquito spray 50% DEET spray
nets and barriers
antimalarial meds

214
Q

metastatic brain cancer can spread from?

A

lung - MC
breast
bowel
skin - namely melanoma
kidney

215
Q

features of brain tumour

A

poss asx

progressive focal neurological symptoms

raised icp

216
Q

features of raised icp

A

headache contant worse at night or on waking or coughing/straining.
vomiting
papilloedema on fundoscopy (paton lines)

altered mental state
ptosis unilateral
visual field defect
3rd and 6th nerve palsy

217
Q

with papilloedema what do u see on fundoscopy?

A

blurring of optic disc margin

engorged retinal veins

haemorrhages around optic disc

paton lines - creases in retina around optic disc

loss of venous pulsation

elevated optic disc

218
Q

what is a glioma?

A

tumour of glial cells in brain/spinal cord.

support/surround neurones.

include: astrocytes,oligodendrocytes, ependymal cells.

grade 1-4.
4 (glioblastoma multiforme)

219
Q

3 types of glioma

A

astrocytoma - mc and aggressive is glioblastoma

oligodendroglioma
ependymoma

220
Q

gliobastoma multiforme

prognosis
imaging
histology
tx

A

solid tumour with central necrosis and a rim that enhances contrast.

pleomorphic tumour cells border necrotic areas

surgery and postop chemo and/or radio.

dex: oedema

221
Q

what is a meningioma?

histology
ix
tx

A

tumour of meninges.
benign
mass effect. = raised icp

arise from arachnoid cap and typically located next to dura.

spindle cells in concentric whirls and calcified psammoma bodies.

CT: contrast enhancement
MRI

tx: RADIO/ SURGERY

222
Q

tell me about pituitary tumours.

press on what?

sx?

mx

A

benign
optic chiasm press - bitemporal hemianopia

cause hormone def or release excessive hormones lead to:
- acromegaly
-hyperprolactinaemia
- cushings disease
- thyroxicosis

transphenoidal surgery
radio
bromocriptine - block excess prolactin
somatostatin analogue - block excess GH

223
Q

symptoms of cerebellar disease

A

D - dysdiadokinesia, dysmetria, “drunk”
A - ataxia - limb,truncal
N - nystagmus - horizantal = ipsilateral hemisphere
I - intention tremor
S - slurred staccato speech, scanning dysarthria
H - hypotonia

224
Q

unilateral cerebellar lesions cause what signs?

A

ipsilateral

225
Q

causes of cerebellar disease

A

friedreichs ataxia

neoplastic: cerebellar haemangioma

stroke
alcohol
ms
hypothyroid
drugS: phenytoin, lead poisoning

paraneoplastic: 2 to lung cancer

226
Q

What is normal pressure hydrocephalus?

A

reversible cause of dementia in elderly.

2 to reduced csf absorption at arachnoid villi.

could be due to head injury, subarachnoid haemorrhage or meningitis

227
Q

classic triad of normal pressure hydrocephalus

A

urinary incontinence

dementia and bradyphrenia

gait abnormality

sx develop over a few months

228
Q

imaging for normal pressure hydrocephalus

A

hydrocephalus with ventriculomegaly in absence of ,or out of proportion to , sulcal enlargement

229
Q

how would you manage normal pressure hydrocephalus

comps of this tx

A

ventriculoperitoneal shunting

seizures
infection
intracerebral haemorrhage

230
Q

What is Cerebral Palsy?

A

non-progressive lesion motor pathways in developing brain.

disorder of movement and posture.

231
Q

causes of cerebral palsy

antenatal

intrapartum

postnatal

A

antenatal 80%
- cerebral malformation
-congenital infection (rubella, toxoplasmosis, CMV)

intrapartum 10% =
- birth asphyxia/trauma
-preterm birth

postnatal 10%
- intraventricular haemorrhage
-meningitis
-head trauma

232
Q

classifying cerebral palsy
4 different types

A

spastic 80%
- hemiplegia, diplegia or quadriplegia
-increased tone (hypertonia) and reduced function resulting from damage to UMN

dyskinetic:
- damage to basal ganglia and substantia nigra
-athetoid movements and oro-motor problems . muscle tone problems (hypertonia/hypotonia) causing the athetoid etc.

ataxic:
- caused by damage to the cerebellum with typical cerebellar signs
- problems with coordinated movement due to above.

mixed: mixed of spastic,dyskinetic and/or ataxic features.

233
Q

patterns of spastic cerebral palsy

A

monoplegia: 1 limb affected

hemiplegia: one side of body affected

diplegia: 4 limbs affected by mostly legs

quadriplegia: neck down all 4 limbs - with seizures, speech disturbance and other impairements

234
Q

what non-motor problems might a cerebral palsy patient have?

A

learning difficulties - 60%

epilepsy 30
squints 30%

hearing impairement 20

235
Q

How would you manage cerebral palsy?

A

tx spasticity:
-oral diazepam
-oral and intrathecal baclofen (muscle relaxant), botulinum toxin type A , orthopaedic surgery and selective dorsal rhizotomy.

anticonvulsants, analgesia prn
physio - stretch and strength muscles prevent muscle contractures.

OT
SLT
DIETICIAN - peg feeding poss?
ORTHO SURGEON - release contractures or length tendons (tenotomy)

glycopyrronium bromide: excessive drooling.
anti-epileptic - seizures

236
Q

what condition makes children at risk of developing cerebral palsy?

A

hypoxic-ischaemic encephalopathy

237
Q

signs and symptoms of cerebral palsy

A

failure to meet milestones

learning difficulty

feeding or swallowing problems

problems with coordination, speech or walking

increased/decreased tone, generally or in specific limbs

hand preference below 18 months .

238
Q

based on neuro exam what to each of these indicate:

hemi/di plegic gait

broad based gait/ataxic gait

high stepping gait

waddling gait

antalgic gait

A

UMN lesion

cerebellar lesion

foot drop/lmn lesion

pelvic muscle weakness due to myopathy

indicates localised pain

239
Q

with a UMN lesion tell me about:

inspection
tone
power
reflexes

A

muscle bulk preserved
hypertonia
slightly reduced
brisk

240
Q

with a lmn tell me about:
inspection
tone
power
reflex

A

reduced muscle bulk with fasciculations
hypotonia
dramatically reduced
reduced

241
Q

complications and associated conditions of cerebral palsy

A

learning disability

epilepsy

kyphoscoliosis

muscle contractures

hearing and visual impairment

gastro-oesophageal reflux

242
Q

what is hypoxic ischaemic encephalopathy?

A

neonates.
hypoxia during birth.

243
Q

causes of HIE

A

anything that leads to asphyxia (deprivation of oxygen) to the brain.

eg:

maternal shock
-intrapartum haemorrhage
-prolapsed cord - causing compression of the cord during birth
nuchal cord - where the cord is wrapped around the neck of the baby

244
Q

grading HIE

mild
moderate
severe

A

sarnat Staging

mild:
- poor feeding, generally irritability and hyper-alert
-resolves within 24 hours
-normal prognosis

moderate:
- poor feeding, lethargic, hypotonic, seizures
-can take weeks to resolve
-up to 40% develop cerebral palsy

severe:
- reduced gcs, apnoeas, flaccid and redcued or absent reflexes
-upto 50% mortality
-upto 90% develop cerebral palsy

245
Q

when to suspect HIE

A

neonate

acidosis (ph under 7) on umbilical abg

poor Apgar score

features of mild,mod,severe HIE

evidence of multi organ failure.

246
Q

how would you manage HIE

A

supportive care with neonatal resus

optimal ventilation, circulatory support, nutrition, acid base balance and seizure tx.

therapeutic hypothermia - protect brain from hypoxic injury.

247
Q

what is horners syndrome?

A

combo of sx that happen when group of nerves known as sympathetic trunk is damaged.
eye and surrounding area on 1 side of face.

248
Q

features of horners syndrome

A

miosis - small pupil

ptosis

enophthalmos - sunken eye

anhidrosis - loss of sweating one side

249
Q

using anhidrosis to decipher where the lesion is for horners syndrome

A

face arm and trunk: central lesion

face: pre-ganglionic

no anhidrosis: post-ganglionic

250
Q

central lesion causes of horners

pre ganglionic

post ganglionic

A

stroke, syringomyelia, ms, tumour, encephalitis

pancoasts tumour , thryoidectomy, trauma, cervical rib

carotid artery dissection, carotid anerusym, cavernous sinus thrombosis, cluster headache

251
Q

heterochronic - difference in iris colour is seen in what?

A

congenital horners

252
Q

horners - what are apraclonidine drops

A

alpha adrenergic agonist

cause pupillary dilation

produces mild pupillary construction in normal pupil.

253
Q

What is epilepsy?

types

A

seizure tendency.

transient episodes of abnormal electrical activity in brain.

generalised tonic-clonic
focal seizures
absence
atonic
myoclonic
infantile spasms
febrile convulsions

254
Q

What are febrile convulsions?

age of onset

mc type of seizure here

clinical features

A

seizures provoked by fever in otherwise normal kids.

6 months and 5 years.

tonic-clonic

usually occur early in viral infection as temp rises rapidly

seizures brief: last less than 5 mins

255
Q

types of febrile convulsion

simple
complex
febrile status epilepticus

A

simple:
- less than 15 mins
-generalised seizure
-typically no recurrence within 24 hours
-should be complete recovery within an hr

complex:
- 15-30 mins
-focal seizure
-may have repeat seizures within 24 hours

febrile status epilepticus :
- over 30 mins

256
Q

Mx of Febrile Convulsion

following a seizure

ongoing

A

admit if first or features of complex seizure

phone ambulance if seizure over 5 mins.

benzodiazepine rescue med: rectal diazepam or bvuccal midazolam

regular antipyretics: dont reduce chance of them occuring

257
Q

prognosis of febrile convulsions

A

risk of another one is 1 in 3. depends on:

age of onset under 18months
fever under 39
shorter duration of fever before seizure
fhx of them

258
Q

rf for developing epilepsy post febrile convulsions

A

fhx of epilepsy

complex febrile seizures.

background of neurodevelopmental disorder

if no rf@ 2.5% risk of developing it.

if kids have all 3 features 50% risk

259
Q

what is benign rolandic epilepsy?

how to ix and what does it show

prognosis

features

A

form of childhood epilepsy occurs between 4 and 12.

EEG - centrotemporal spikes

excellent prognosis - seizures stop by adolescence

seizures at night.
partial seizures (paresthesia affect face) but secondary generalisation may occur (parents may only report tonic-clonic movements)

260
Q

Using Contraception in epilepsy what factors are to be considered?

A

effect of contraceptive on effectiveness of anti-epileptic

effect of anti-epileptic on effectiveness of contraceptive

potential teratogenic effects of anti-epileptic if women becomes pregnant

261
Q

if women is taking phenytoin carbamazepine barbiturates primidone topiramate oxcarbazepine what to do?

for contraception in epileptic pt

A

ukmec 3 : the COCP and POP

ukmec 2 : implant

ukmec 1 : depo-provera, IUD,IUS

use condom

if COCP : min of 30 ug of ethinylestradiol

262
Q

for lamotrigine if women takes what to do?

contraceptionin epileptic pt

A

use condom

ukmec 3 : cocp
ukmec 1: pop, implant, depo-provera, Iud, ius

if COCP: min or 30 ug of ethinylestradiol

263
Q

what conditions are associated with epilepsy?

A

cerebral palsy: 30% have it

tuberous sclerosis

mitochondrial diseases

264
Q

what is an alcohol withdrawal seizure?

mechanism

tx

A

pt hx of alcohol excess suddenly stopped drinking.

36 hours after drink cessation.

give benzodiazepine after stopping.

chronic alcohol enhances gaba mediated inhibition in cns and inhibits nmda-type glutamate receptors.

alcohol withdrawal dose the opposite

265
Q

what are psychogenic non-epileptic seizures?

A

pseudoseizures

epileptic-like seizures but no electrical discharges.

hx of mental health or personality disorder

266
Q

define a focal seizure

A

partial seizure.- start in temporal lobe.

start in a specific area , one 1 side of brain.

varied awareness.

30 yr old women told by her husband she wakes at night, grunting sound, lip smacking, non responsive during ep. after minute falls asleep again.

focal impaired awareness - explained above.

classified into
motor: jacksonian march

non-motor : deja vu, jamais vu

or other features like aura

sx: affect hearing speech memory and emotions.

hallucinations
-memory flashbacks
-deja vu
doing strange things on autopilot

267
Q

generalised seizure define

A

involve networks on both sides of the brain at onset.

lose conciousness immediately.

motor: tonic clonic
non motor: absence

specific types:
-tonic clonic - grand mal
- tonic
-clonic
-typical absence - petit mal
- myoclonic: brief,rapid muscle jerks
- atonic

268
Q

unknown onset seizure - what is it?

A

unknown origin of seizure

269
Q

focal to bilateral seizure - what is it

A

starts on 1 side of brain in specific area before spreading to both lobes

previously called secondary generalised seizure

270
Q

tell me about typical absence seizures: petit mal

onset

duration

eeg

tx

prognosis

A

onset: 4-8 years

duration : few-30 seconds. no warning, quick recovery: often many per day

eeg: 3Hz, generalised, symmetrical

sodium valproate, ethosuximide

good prognosis: 90-95% become seizure free in adolescence

271
Q

if a focal seizure happens starts in occipital lobe (visual) what happens?

A

floaters/flashes

272
Q

if a focal seizure happens in parietal lobe what happens ? (sensory)

A

paresthesia

273
Q

if a focal seizure happens in frontal lobe? (motor)

A

head/leg movements, posturing
post-ictal weakness (todd’s paresis),

jacksonian march (clonic movements travelling proximally)

274
Q

if a focal seizure starts in temporal lobe what can i expect?

A

last around 1 min - automatisms (lip smacking/grabbing/plucking) common

with/without impairement of conciousness or awareness

aura in most:
- rising epigastric sensation
-psychic or experiental phenomena like deja vu , jamais vu
-less common: hallucination (auditory,gustatory,olfactory)

275
Q

sodium valproate is associated with what issue for maternal kids?

A

neural tube defects

risk of neurodevelopmental delay in kids after maternal use of it.

DONT USE IN PREGNANCY AND WOMEN OF CHILDBEARING AGE UNLESS NECESSARY.

276
Q

which of the epileptic drugs is seen as least teratogenic or older antiepileptics?

A

carbamazepine

277
Q

phenytoin is associated with what issue?

antiepileptic

what to give with it. this is to prevent what?

A

cleft palate

vit k
last month of pregnancy
prevent clotting disorders in newborn

278
Q

is breast feeding safe for mothers taking anti-epileptics?

is there an exception to the rule?

A

yes
NO BARBITURATES

279
Q

women want to get pregnant epileptic what should they take and why?

A

folic acid 5mg per day well before pregnancy

minimise risk of neural tube defects

280
Q

briefly explain what an absence seizure is?

tx

A

in kids.

pt becomes blank stares into space and abruptly returns to normal.

unaware of surroundings, wont respond.

10-20 seconds.

stop when they get older

1st line: ethosuximide
2nd line:
m - sodium valproate
f: lamotrigine or levetiracetam

carbamazepine - exacerbate absence seizures

281
Q

how would you tx focal seizures ?

A

1st line : lamotrigine or levetiracetam

2nd line: carbamazepine, oxcarbazepine or zonisamide

282
Q

the rules are you start antiepileptics after second seizure.

in what case would you start after first?

A

pt has neuro deficit

brain imaging shows structural abnormality

EEG shows unequivocal epileptic activity.

pt or their fam or carer consider the risk of having a further seizure unacceptable

283
Q

generalised tonic clonic seizure tx?

A

male: sodium valproate

female: lamotrigine or levetiracetam

under 10, unlikely to need tx when old enough to have kids or women unable to have children can be given sodium valproate first line.

284
Q

how to atonic seizures present?

tx?

A

drop attacks.

brief lapse in muscle tone.

no more than 3 minutes.
childhood begin.

indicative of lennox-gastaut syndrome.

mx:
- m: sodium valproate
- f: lamotrigine

285
Q

how do myoclonic seizures present?

tx?

A

sudden brief muscle contractions - sudden jump.

awake during.

happen in kids as part of juvenile myoclonic epilepsy.

tx:
- m - sodium valproate
- f : levetiracetam

286
Q

rescue medication for epilepsy if they dont terminate spontaneously ie after 5-10 mins

A

benzodiazepines like diazepam

administer rectally or intranasally/under tongue.

if still fits: status epilepticus. - medical emergency - hospital tx required.

mx: further benzodiazepine med, infusion of antiepileptic or general anesthetic.

287
Q

ix for epilepsy

A

good history

eeg: typical patterns of it. after the second simple tonic clonic do.

MRI brain: structure of brain.

ecg - exclude heart problems

blood electrolytes - sodium, potassium, calcium , magnesium

bg: hypoglycaemia and diabetes

blood cultures, urine cultures and lp where sepsis, encephalitis or meningitis is suspected

288
Q

general advice for epileptic patients

A

take showers not baths

cautious with heights, traffic, heavy/hot/electric equipment

be very catious with swimming unless seizures well controlled and they are closely supervised.

289
Q

mx of seizures physically

A

pt in safe position - carpeted floor

recovery position if poss

something soft under head

remove obstacles that could lead to injury

note the time at start and end

call ambulance if more than 5 mins or 1st seizure.

290
Q

what is status epilepticus?

mx:

medical options in community ?

A

med emergency

seizure lasting more than 5 mins or 2 or more seizures without regaining consciousness in interim.

ABCDE approach
secure airway
high conc ox
assess cardiac and resp function
check bg levels
iv access - insert cannula
iv lorazepam - repeated after 10 mins if the seizure continues.

if persist final step is iv phenobarbital or phenytoin. intubation and ventilation to secure airway- transfer to icu.

med options in community:
- buccal midazolam
- rectal diazepam

Phase 3a Finals (26 decks)

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