Neurological Conditions Flashcards

Question 1

Q

What is Bell’s Palsy and what is the typical patient

Answer

A

Acute unilateral peripheral facial nerve palsy (pt examination and history are unremarcable).
Deficits affect all facial zones equally on one side that fully resolve within 72 hours

15-40 year old individual, may have had an upper respiratory tract infection recently or has HSV-1.
Also common in pregnancy

Question 2

Q

What are the clinical features of Bell’s Palsy

Answer

A

Unilateral facial weakness and droop

Non-forehead sparing - shows its ipsilateral LMN lesion (if was forehead sparing then means a contralateral UMN lesion like stroke)

Involves all nerve branches equally

Dry eye and mouth - keratoconjunctivitis cicca

Loss of taste on anterior 2/3 of tongue

Hyperacuisis (sensitive to noise)

involuntary and abnormal movements of face

Question 3

Q

How is Bell’s Palsy investigated

Answer

A

Electromyography

Question 4

Q

WHat is the management of Bell’s Palsy

Answer

A

Corticosteroids within 72 hours (oral prednisolone)

Eye protection- lid taping or lubricating eye drops- dry eye is common and can lead to keratopathy

If no improvement in 3 weeks- ENT referral

If severe then- surgical decompression and antivirals like acyclovir

Question 5

Q

What are the complications and prognosis of Bell’s Palsy

Answer

A

Comp- keratoconjunctivitis sicca, eye infection, eye ulcers

Prognosis- 85-90% recover function within 2-12 weeks with or without treatment. may be some permanent weakness or paralysis

Question 6

Q

What is a brain abscess, whats the cause and what is the most typical patient

Answer

A

A suppurative (pus discharging) collection of microbes (bacterial, fungal or parasitic) within a gliotic capsule occuring within the brain parenchyma

Cause- spread of an infection (otitis media, sinusitis, dental infection, meningitis, ednocarditis) trauma (penetrating head injuries) or surgery to the scalp

Man over 30 infected with viridans streptococci because had sinusitus. Or infected with staph aureus
Children 4-7 year old

Question 7

Q

What are the clinical features of brain abscesses

Answer

A

Raised ICP- nausea, vomiting, papilloedema, seizures

Dull persistent headache (rupture usually suddenly worse and due to meningitis)

Focal neurology- 3rd or 6th nerve palsy. Usually 6th nerve palsy (if right eye lesion then when looking forward right eye looks adducted toward nose) 3rd would cause right eye to be down and out

fever

Psotitive kernig - lie down- leg in table top position and extend - if have pain then positive
Positive brudzinski sign- move head up to chest- they involuntarily move their knee and hip to flexed

Question 8

Q

What are the investigations for brain abscesses

Answer

A

MRI with contrast- see ring enhancing lesions

CT head with or without contrast

Elevated ESR and CRP

Biopsy is best to confirm

Question 9

Q

What is the management plan of brain abscesses

Answer

A

Craniotomy to debride the abscess cavity

IV Antibiotics (ceftriaxone)+ metronidazole+ vancomycin)

ICP management - dexamethosone

Anticonvulsants

Question 10

Q

What are the complications and prognosis of brain abscesses

Answer

A

Comp- seizure, hydrocephalus, hyponatraemia, death

Prognosis- mortality under 13%. presenting neurological status if the major prognistic factor

Question 11

Q

What are the most common cancer causes of brain metastases

Answer

A

Most common= LUNG cancer
breast, colorectal, testicular too

Question 12

Q

What are the clinical features of brain metastases

Answer

A

Persistent headache- worse in morning and when lying down (is suggestive of ICP- aka something taking up space in brain)

Seizures

Focal Neurological changes- speech, vision, hearing

Cognitive deficits

CN6 palsy- medially diverted eye and diplopia

Question 13

Q

What investigations should be carried out if a brain metastases is suspected

Answer

A

Imaging- CT or MRI

If headache worsening and higher cognitive function impairment then MRI

Question 14

Q

What is the management of brain metastases and what is the prognosis

Answer

A

1st- high dose dexamethososne (to reduce oedema)
If limited metastases- surgical resection
If extensive then - stereotactic radiosurgery, whole brain radiation therapy or chemotherapy

Prog- 1 month without treatment, less than 1 year with

Question 15

Q

What is chronic fatigue syndrome

Answer

A

also known as myalgic encephalomyelitis

Diagnosed after 4 months of disabling fatigue affecting mental and phyical function more than 50% of time but has no other disease

Female 3x more likely than males. onset usually during adolescence and between 30-50 years old

Question 16

Q

What are the clinical features of chronic fatigue syndrom

Answer

A

Persistent Disabling Fatigue- can be for more than 6 months, has to be at least 4 to diagnose

Post-exertional fatigue- exhaustion and impairment following minimal physical or congitive effort

Short term memory/concentration impairment

Sore throat

Arthralgia- joing stiffness

Headache

Unrefreshing sleep

Flu like symptoms - malaise, myalgia, fever

painful lymph nodes

Question 17

Q

What investigations should be done if chronic fatigue syndrome/myalgic encephalomyelitis is suspected

Answer

A

DePaul Symptom Questionnaire- screening

Exclude others:
FBC, U&E, LFT, glucose, TFT, ESR, CRP, calcium, CK, ferritin, coeliac screening
Urinalysis

Question 18

Q

What is the management for chronic fatigue syndrome/ myalgic encephalomyelitis

Answer

A

Individualised therapy- manage symptoms to improve functional capacity includes
-CBT
-Graded excersise therapy
-Low dose amitriptyline
-Referral to pain management clinic
-Mindfulness, sleep hygiene, occupational therapy

Question 19

Q

What are the complications and prognosis of chronic fatigue disorder/myalgic encephalomyelitis

Answer

A

Major depressive disorder

17-60% improve but less than 10 full recover, 20 worsen

Question 20

Q

What is encephalitis, who is mostly at risk and what is the cause

Answer

A

Inflammation of the brain parenchyma.

RF
BIMODAL age distribution - younger than 1 years old and older than 65 most likely.
Immunosuppressed
Viral infectios
body fluid exposure
Organ transplantation
Animal or insect bites
Travel
Season

Cause- due to infection. Usually viral and HSV-1 (Herpes Simple Virus Type 1) is the most common. Can also be to bacterial, fungal or parasitic or in immunocompromised patients or pt that have autoimmune/paraneoplastic syndromes.

Question 21

Q

What is the clinical presentation of encephalitis

Answer

A

normally mild
altered mental state- SUDDEN change in behaviour
fever + malaise
flu like prodromal illness
rash
focal neurological deficit- aphasia(difficult speaking), hemianopia(loss of half of sight), hemiparesis (weakness of muscles), loss of consciousness, seizures
travelled

Raised ICP- Cushing triad (bradycardia, irregular breathing, widened pulse pressure) also papilloedema

Question 22

Q

What are the investigations if encephalitis is suspected

Answer

A

CSF Analysis (lumbar puncture): high lymphocytes, high protein, normal glucose
- viral: lymphocytes predominate (granular appearance)
- bacterial: neutrophils predominate (many nucleus lobes)
CSF Viral PCR- t confirm presence of HSV
- Do CT prior to lumbar puncture to exclude raised ICP. If CT head shows temporal lobe changes= HSV-1 encephalitis

Bloods: high WBC, hyponatraemia, high LFTs

Blood culture- detect bacterial infection

Throat swab- detect virus

MRI/CT Brain: exclude mass lesion, CT brain may show temporal head changes of HSV, MRi will show brain swelling and increased brain signal

Question 23

Q

What is the management of encephalitis

Answer

A

Viral or confirmed HSV= IV acyclovir + supportive care

Non-viral encephalitis= ABs for bacteria and supportive care

Supportive care= intubation, ventilation, circulation and electrolyte support

Question 24

Q

What are the complications and prognosis of encephalitis

Answer

A

COMP-
death
seizures
hypothalamic dysfunction like diabetes insipidus (too little ADH so pee a lot) or SIADH (Syndrome of inappropriate antidiuretic hormone secretion- too much ADH so concentrated urine)

Prog- poor

Question 25

Q

What is epilepsy, criteria to be classified as epilepsy

Answer

A

Neurological condition characterised by recurrent seizures (excessive activity of cortical neurones resulting in transient neurological symptoms)
Has to have more than 2 seziures more than 24 hours apart for diagnosis

Question 26

Q

What are the causes of epilepsy

Answer

A

Primary= idiopathic

Secondary=
tumour
meningitis
vasculitis
alcohol withdrawal
haemorrhage
metabolic

Conditions linked- cerebral palsy, tuberous sclerosis, mitochondrial disease

Question 27

Q

What are the types of seizures

Answer

A

Focal- localised to specific cortical regions, can be complex (consciousness affected) or non-complex (consciousness not affected)
Simple focal seizures: twitching or a change in sensation, such as a strange taste or smell.
Complex focal seizures :confused or dazed, unable to respond to questions or direction for up to a few minutes.

Generalised seizure- affects whole brain, consciousness lost immediately. 5 types
- absence: rapid blinking or stare into space
- tonic: Muscles in the body become stiff.
- atonic: Muscles in the body relax.
- tonic-clonic: stiff then jerking/spasm movements, may cry out and fall.
-myoclonic: Periods of shaking or jerking parts on the body.

Status epilepticus
a seizure lasting longer than 5 mins, or 2 or more seizures within a 5 minute period without the person retuning to normal inbetween.
Have to rule out hypoxia and hypoglycaemia thru blood gluose

Question 28

Q

What are the clinical features of epilepsy

Answer

A

FOCAL SEIZURE
- frontal: motor convulsions, post-ictal flaccid weakness, jacksonian march (clonic movements starting in one extremity then spreads e.g. in little finger twitching/tingling up arm)

frontal lobe complex- loss of consiousness, involuntary actions, rapid recovery
Temporal lobe seizure features?
Aura- involving: Weird smell, iInvoluntary movements, Deja vu, Abdo pain
Lip smacking/plucking/grabbing (automatisms)
Post-ictal dysphasia
Hallucinations
Occipital lobe seizure
Visual disturbances (flashers and floaters)
Parietal lobe seizure
Sensory issues (paraesthesia- tingling, numbness)

GENERALISED SEIZURES
- Tonic-clonic seizure
Vague symptoms before attack e.g. irritability
Tonic phase (generalised muscle spasm- goes stiff and falls to floor)
Clonic phase (repetitive synchronous jerks- jerking limbs or loss of bladder control)
Urinary incontinence
Tongue biting
Post-ictal phase
- Impaired consciousness
- Lethargy
- Confusion

Absence seizure
Onset in childhood
Loss of consciousness but maintained posture (don’t fall down)
No post-ictal phase
Often begins abruptly without warning and ends abruptly
Patient has no recollection of episode
Stares blankly into space
EEG shows 3 Hz spike and wave
Myoclonic seizure
convulsions without the muscle tensing (tonic phase)
Sudden jerking of limb, trunk or face with preserved consciousness
Atonic seizure
sudden muscle relaxation causing patients to fall to the ground and then may motionless
incontinence
post-ictal confusion
Tonic seizure
muscle tensing without convulsions (clonic phase)

Question 29

Q

What investigations are done for epilepsy

Answer

A

Clinical diagnosis- 2 or more 24 hours apart

EEG- confirm diagnosis and classify
MRI- check for structural, space occupying or vascular lesions that may cause midline shift.

Bloods- capillary blood glucose (exclude hypoglycaemia), electrolytes (hypocalcaemia and hyponatraemia), prolactin (seizure vs psudoseizure)

Question 30

Q

What is the management of epilepsy

Answer

A

only start treatment after more than 2 unprovoked seizures

FOCAL
1st- lamotrigine or levetiracetam
2nd- carbamazepine

GENERALISED SEIZURES (NOT ABSENCE)
- Men: sodium valporate
-Women: lamotrigine (levetiracetam if myoclonic)

ABSENCE
1st: Ethosuximide
Men 2nd- sodium valporate
Women 2nd- lamotragine/levetiracetam

STATUS EPILEPTICUS
Hospital- IV lorezapem
Community- PR diazepam
If doesnt work another dose of IV lorezapem, if that doesnt work then IV phenytoin
MAX 2 DOSES OF BENZODIAZEPINES

DVLA
1st unprovoked seizure= 6 months off driving
abnormal brain image or eeg= 12 months off driving

Question 31

Q

What are the complications and prognosis of epilepsy (inc comp of drugs)

Answer

A

COMP:
fractured from tonic-clonic
behavioural problems
sudden death
complications to anti-epileptic drugs
-Lamotrigine= can cause steven johnson syndrome, large blistering rash over body
-Carbamazipine= SIADH, drowsiness, steven johnsons syndrome, neutropenia, osteoporosis
-sodium valporate: weight gain
-phenytoin= gingival hypertrophy, peripheral neuropathy

Prognosis- 50% remission at 1 year

Question 32

Q

What is an essential tremor

Answer

A

Progressive, mainly symmetrical, rhythmic, involuntary oscillation movement disorder of the hands and forearms. Absent at rest, present during posture and intentional movements
Bimodal distribution- teens and elderly
Family history - as its autosomal dominant inheritance

Question 33

Q

What are the clinical features of essential tremor

Answer

A

Bilateral upper limb action tremor- absence of other neurological signs
Worse with sustained voluntary movement like outstretched arms, stress or anxiety
90% hands, head 30%, voice 15%
may have intention or resting tremor
improves with alochol consumption

Question 34

Q

What are the investigations of essential temor

Answer

A

clinical diagnosis alone

Question 35

Q

What is the management plan for essential tremor

Answer

A

if no dysfunction/mild- just observation
If dysfunction- 1st line propranolol or primidone. 2nd line gabapentin.
If both drugs have no effect then Deep Brain Stimulation

Question 36

Q

What are the complications and prognosis of essential tremor

Answer

A

Comp- DBS complications like hameorrhage or infection
Prog- persistant and preogressive condition, many mild cases dont seek treatment

Question 37

Q

What is malaria, what are the risk factors

Answer

A

Parasitic infection caused by the protozoa of the genus plasmodium- plasmodium falciparum is most life threatening
is a NOTIFIABLE DISEASE
Tropical and subtropical regions- travellers account for most cases in western countries
Bite by an infected female anopheles mosquito OR blood tranfusion OR organ transplantation

RF- travel to an endemic area (african countries), inedequate chemoprophylaxis, not using insecticide-treated bed net in endemic areas

Protective factors - sickle cell anaemia, G6PD deficiency

Question 38

Q

What is the clinical presentation of malaria

Answer

A

Cyclical fevers with chills and rigors (shivering)- aka sever cold/rigors followed by severe sweating, alternates days
Haemolytic anaemia- causes jaundice and may turn urine dark
Splenomegaly
Headache
Weakness
Myalgia
Arthralgia
Anorexia
Diarrhoea

Question 39

Q

What are the investigations of malaria

Answer

A

Giemsa stained thick and thin blood smears- detects asexual or sexual forms of the parasites inside erythrocytes
Thick- detects parasites present
Thin- detects species

FBC- check for anaemia

Rapid Diagnostic Tests- detect parasite antigen or enzyme

Question 40

Q

What is the management of malaria

Answer

A

Chloroquine (ok if preg) or Hydroxychloroquine
Primiquine once symptoms resolve to presvent relapse
Prevention- avoid exposure use nets, repellant, protective clothing and prophylaxis

Question 41

Q

What are the complications and prognosis of malaria

Answer

A

Comp:
AKI- dehydration and hypovolaemia
Hypoglycaemia
Metabolic acidosis
Severe anemia
Seizures
ARDS

Prog- sever if low host immunity, pregnant, younger than 5, immunocompromised, older adults

Question 42

Q

What is meningitis and the risk factors

Answer

A

Infection of the meninges in the brain or spinal cord, commonly viral or bacterial- may be fungal parasitic or due to noninfectious cause
Less than 1 years old or 43 years old
RF- immunocompromised, crowded living conditions, otitis media, sinusitis, CSF leak after head trauma or neurosurgery, sepsis

Question 43

Q

Describe the different causes (organism wise) of meningitis

Answer

A

BACTERIAL (serious)
- Neonates: Group B streptococcus (extended labour, infection in previous pregnancy). Listeria monocytogenes
- Children- Streptococcus pneumoniae (Gram+ diplococci)(PNEUMONIA = POSITIVE) or neisseria meningitidis (Gram - diplococci, causes non-blanching rash) (NEISSERIA NEGATIVE NON BLANCHING)
-Elderly- sterptococcus pneumoniae (gram +). Listeria monocytogenes

VIRAL (common)
- Enteroviruses (poliovirus, coxsakie) : most common cause
HSV
VZV
mumps

Question 44

Q

What are the clinical features of meningitis

Answer

A

bacterial + viral similar but VIRAL is LESS ACUTE and usually self limiting within 7-10 days
Triad- fever, headache, neck stiffness
Photophobia
Nausea and Vomiting
Altered mental state
seizures
Deafness
Meningococcal meningitis= non blanching rash
Kernig sign- cant straighten leg when hip flexed to 90
Brudzinski sign- forced flexion of neck result in reflex flexion of hips

Neonates: lethargy, irritability, poor appetite, vomiting, fontanelle bulging, seizures

Question 45

Q

What are the investigations for meningitis

Answer

A

CT head first (before lumbar puncture) if increased ICP is suspected as LP can cause sudden decrease in pressure and lead to brain herniation

Lumbar puncture- CSF analysis (only is no signs of riased ICP - vomiting, blurred vision, headache, less alert)
- BACTERIAL: ““cloudy””, ““high neutrophils”” (granular), high protein, ““LOW glucose””, normal openig pressure
- VIRAL: ““clear””, ““high lymphocytes””, normal/high protein, normal glucose, normal opening pressure
- TB: ““slightly cloudy/fibrin web””, ““high lymphocytes””, high protein, ““LOW glucose””, ““high opening pressure””

Blood Cultures: obtain 2 sets before antibiotic therapy

Question 46

Q

What is the management plan of meningitis

Answer

A

Primary care- as soon as suspected IV or IM Benzylpenicillin or IV/IM cefotaxime or ceftriaxone and send to hospital

If LP contraindicated (sepsis/evolving rash sign, severe resp/cardiac compromise, signifiant bleeding risk, raised ICP sign ( papulloedema, neurological sign, seizure, GCS 12 or less) then:
-Bloods
- Immediate IV ABs : cefotaxime or ceftriaxone (if theyre over 50yrs old then add amoxicillin)
- IV Dexamethosone shortly before or with first dose of ABs (reduces complication risk)
- If ICP raised: secure airway + high flow oxygen, bloods and blood cultures from IV, IV dexamethosone, IV ABs, Do CT scan)

If LP isnt contraindicated
-Bloods and blood culures
-LP without CT
- Immediate IV ABs : cefotaxime or ceftriaxone (if theyre over 50yrs old then add amoxicillin)
- IV Dexamethosone shortly before or with first dose of ABs (reduces complication risk) AVOID in meningococcal septicaemia
- Viral- supportive measures as usually self limiting (maybe antiviral)

Close contacts:
-Prophylactic ABs to close contacts of meningococcal meningitis - oral ciprofloxacin or rifampicin

SUSPECTED Bacterial meningitis
Over 3 moths- IV ceftriaxone. Dexamethasone
Lower than 3 months- IV cefotsxime plus amoxicillin (can give caftriaxone IF no jaundice, not premature, normal albumin, no acidosis, no calcium containing infusions)
If travelled abroad- vancomycin
WHEN CALCIUM- cefotaxime not ceftriaxone

CONFIRMED BACTERIAL
Younger than 3 months:
Group B- IV cefotaxime
Listeria Monocytogenes- IV amoxicillin and gentamicin (gentamicin for first 7 days only)
Gram negative bacilli: cefotaxime

Older than 3 months:
H influenza - IV cefatriaxone
Pneumoniae (same)

UNCONFIRMED BACTERIAL MENINGITIS
younger than 3 months- cefotaxime plus amoxicillin
Over 3 months- ceftriaxone

MENINGOCOCCAL
IV ceftriaxone 7 days
If only suspected then do the same

Question 47

Q

What are the complications and prognosis of meningitis

Answer

A

Comp- deafness, spticaemia, shock, disseminated intravascular coagnulation, cerebral oedema, renal failure, cranial nerve lesion

Prognosis-
Bacterial is fatal untreated
Viral resolves spontaneously mostly

Question 48

Q

What is a migraine, the types of migraine and its risk factors

Answer

A

Chronic, episodic neurological disorder that has a strong genetic component and usually presents in early to mid life.

Primary headache characterised by recurrent episodes of unilateral localised pain

F:M 3:1

Adolescence and early childhood

Three types:
-migraine with aura (classic migraine)
- migraine without aura (common migraine)
-migraine variant (familial hemiplegic, opthalmoplegic)

Risk Factors: FHx migraine, female, menstruation, stress, obesity, sleep disorders, medication overuse,

Triggers (CHOCOLATE)
Chocolate
Hangovers
Orgasms
Cheese/Caffiene
Oral Contraceptive
Lie ins
Alcohol
Travel
Exercise

Question 49

Q

What is the clinical presentation of migraines

Answer

A

Prolonged unilateral headache- 4-72hours, recurrent episodes
Throbbing/pulsatile pain
Nausea
Aura before- flashing lights
Photophobia and Phonophobia- quiet dark room needed
Headache worse with activity
Decreased ability to function (affects daily activity)
Abdominal pain associated in children

Question 50

Q

Describe the three types of headache and their treatment

Answer

A

Migraine: Unilateral, 4-72 hr, pulsing throbbing pain with nausea, photophobia or phonophobia. may have aura
T- NSAIDs, tripatan.
Prophylaxis- lifestyle change, B blockers, topiramate

Tension: Bilateral, over 30 min, band like pain, no photophobia or phonophobia or aura
T- analgestic, NSAID, acetaminophen
Prophylaxis- TCA (amitryptaline)

Cluster: Unilateral, 15min-3hr, periorbital pain with lacrimation and rhinorrhea. Horner syndrome maybe
T- sumatriptan, 100% O2 therapy
Prophylaxis- verapamil

Question 51

Q

What investigations are done if migraine is suspected

Answer

A

Clinical diagnosis by history and physical exam

Can do:
ESR (raised in temporal arteritis)
Lumbar puncture (SAH or meningitis)
MRI or CT brain

Question 52

Q

What is the management plan for migraines

Answer

A

ALL PT : Limit stimuli (light and noise) and activity.
Nausea with IV fluids and anti-emetics (metoclopramide)

1st line - oral triptan (sumatriptan)+ NSAID
- dont use triptan with coronary artery disease patients as can cause coronary vasospasm
- 12-17 year olds can have nasal triptans rather than oral

Prophylaxis (more than 2 per month)= propanolol or topiramate
- Propanolol avoided in asthmatics bcs bronchoconstriction
- Propanolol preferred in pregnant women and women of child bearing age as topiramate can cause cleft lip

Medicine for headaches can trigger medication overuse headaches if so then:
-Stop all medication including: simple analgesia: paracetomol, NSAIDs + triptans
- If was on opioid then withdraw gradually

Pregnant pt:
1st Paracetomol
2nd NSAIDs in first and second trimester
Avoid aspirin and opioids in pregnancy

Individuals that have migraine with aura should not have combined pill

Question 53

Q

What are the complications and prognosis of migraines

Answer

A

Inc risk of pre-eclampsia
Inc risk of depression
Analgesia overuse headaches

Prog- most do well

Question 54

Q

What are the clinical features of cluster headaches

Answer

A

Intense sharp stabbing pain around one eye
1-2 times per day 15min to 2 hours
restless and agitated during attack as severe
Clusters last 4-12 weeks
redness, lacrimation, lid swelling
Nasal stuffiness
Miosis and ptosis - horners syndrome

Question 55

Q

What investigation is needed if cluster headache is suspected

Answer

A

MRI with gadolinium contrast

Question 56

Q

What is the treatment of cluster headaches

Answer

A

Subcut triptan and 100% O2 therapy

Triptan not to be used if have coronary artery diseasr

Prophylaxis: verapamil

Question 57

Q

What is motor neurone disease and the types

Answer

A

Neurodegenerative disease with upper and lower motor neurone dysfunction
Males, over 65
FHx of ALS in 5-10% of cases
Cause unknown

Types:
1) Ayotrophic lateral sclerosis- UMN and LMN signs
2) Progressive muscular atrophy- only LMN signs, best prognosis
3) Primary lateral sclerosis- UMN signs only
4) Prograssive bulbar palsy variant- tongue and bulbar involvement (dysarthria, dysphagia) - worst prognosis

Those with MND at risk of developing frontotemporal dementia

Question 58

Q

What are the clinical features of motor neurone disease

Answer

A

Progressive muscle weakness
Fasciculations
Dysphagia- bulbar onset ALS may present with difficulty swallowing
Shortness of breath
Eye movements spared, normal sensation
Wasting of thenar muscles and wasting of tongue base

UMN sign- spasticity, hyper-reflexia, clonus, positive babinski sign, brisk limb and jaw reflex, dysarthria, dysphagia, loss of dexterity
LMN sign- hypotonia, hyporelexia, muscle atrophy, tongue fasciculations and fibrillations , dysphagia, weakness, nasal speech

Assymetrical symptoms

Question 59

Q

What investigations are used if MND is suspected

Answer

A

Clinical diagnosis assess history and examination

Electromyography EMG- show denervation
Normal nerve conuction studies to rule out neuropathy
MRI- exclude cord compression

Spirometry to monitor respiratory muscle weakness

Question 60

Q

What is the management plan of MND

Answer

A

1st line- Riluzole a glutamate agonist, prolongs life by 3 months

Repiratory care- BIPAP (NIV) at night for type 2 resp failure

Percutaneus gastronomy (PEG) tube if difficulty swallowing and poor nutrition

Question 61

Q

What are the complications and prognosis of MND

Answer

A

COMP:
Respiratory failure
Nutritional deficit
Aspiration pneumonia
Fronto-temporal dementia

Prog: die within 3-5 years

Question 62

Q

What is multiple sclerosis

Answer

A

Chronic degenerative disease of the CNS caused by immune-mediated inflammatory processes. Results in demyelination and axonal degeneration in the brain and spinal cord.
Dissemination in time and space- lesions in the CNS must have occurred in at least 2 different places and at least 2 different times.
Female3:Male1, 20-40 years old, white people (young white female)

Three forms:
1) Relapsing-remitting - Acute attacks last 1-2 month with complete recovery inbetween
2) Secondary progressive disease- A relapsing remitting patient who has deteriorated and developed neurological signs and symptoms between relapses
3) Primary progressive MS- Progressive deterioration from onset, no remission/relapse period

Cause: genetic prediscposition, environmental risk factors ( low vitamin D, smoking, EBV)

Question 63

Q

What are the clinical features of Multiple sclerosis

Answer

A

Optic neuritis: first manifestation, unilateral impaired vision, colour blindness, pain in moving eye, RAPD (both pupils illuminated in swinging flashlight test

Intrauclear opthalmoplegia- lesion of the medial longitudinal fasciculus blocking connection between contralateral 6th nerve nucleus and ipsilateral 3rd nerve nucleus affecting horizontal gaze
- Ipsilateral impaired adduction (temporal) e.g. right MLF lesion so right eye cant look at nose
- Nystagmus in eye abducting (moving nasally) e.g right MLG lesion so left eye can still abduct (look temporally) by is shaky

Headache and fatigue

Sensory disturbances (patchy paraesthesia)

Weak after walking

UMN signs- positive babinski, spasticity, hyperreflexia

Leg cramping

Bladder disorders (urinary incontinence)

Lhermittes sign- paraesthesia in limbs on neck felxion

Hoffmans sign- flicking/putting pressure on nail bed causes twitching of thumb of thumb or fingers

Unthoffs phenomenon- neurological symptoms are exacerbated by inc in body temp e.g. after hot baths or exercise

Question 64

Q

What are the investigations for multiple sclerosis

Answer

A

MRI Brain with contrast- view demyelinating lesions, more white/translucency around the ventricles

MRI Spinal cord with contrast : see white blob in middle of spinal cord

Lumbar Puncture + CSF Examination - oligoclonal bands+ elevated levels og IgG antibodies

Visually Evoked Potentials- optic neuritis leads to demyelination of optic nerve so slower conduction times = prolonged visually evoked potential

Answer 65

A

For relapse as steroids dont help when return to baseline just shorten relapse:
1st- IV glucocorticoids (methylprednisolone)
2nd- plasma exchange

Reduce risk ofelpasing:
Immunomodulators (beta-interferon) or natalizumab

Spasticity: baclofen or gabapentin

Answer 66

A

COMP:
UTI
Osteopenia+ Osteoporosis
Depression
Visual Impairment
Erectile Dysfunction
Cognitive Impairment
Impaired Mobility

Prognosis:
hgih relapse rate in first 2 years after onset

Answer 67

A

Autoimmune neuromuscular disease characterised by generalised muscle weakness

Cause: Autoantibodies against post-synaptic nicotinic Ach receptors (AChR) at the neuromuscular junction

F>M

Associated with thymomas (tumour of anterior mediastinum and thymic hyperplasia. Thymomas can cause SVC obstruction

RF- other autoimmune conditions

Answer 68

A

Muscle fatiguability- worse with activity, improves on rest (so worse at end of day)
Ptosis and diplopia
Dysphagia - difficult swallowing
Dysarthria - changes in speech
Facial Paresis
Proximal Limb weakness
Respiratory Muscle weakness- lead to dyspnoea

Answer 69

A

Serum AChR antibody analysis- positive is specific for myasthenia gravis

Electromyography (EMG)- shows decremental response to repetitive nerve stimulation. most Sensitive test

CT thorax-look for thymoma

Muscle specific Tyrosine Kinase antibodies- positive

Tensilonn test- IV edrophonium reduces muscle weakness temporarily. Not used much bcs cardiac arrythmia risk

Answer 70

A

Beta blockers can make worse, can cause FVC to drop due to muscle weakness

Answer 71

A

1st- Long acting acetylcholinesterase inhibitors (pyridostigmine). If take too much then cholinergic crisis (too much ACh= cramps, increased salivation, lacrimation, muscular weakness, paralysis, muscular fasciculation, diarrhea, and blurry vision)

Corticosteroids (prednisolone) if symptoms dont resolve

Acute myasthnic crisis = plasma exchange/plasmapheresis and IV immunoglobulins

Surgery- thymectomy : minimise need for immunosuppressants

AVOID BETA BLOCKERS

Answer 72

A

COMP:
Myasthenic crisis ( give plasmapheresis and IV immunoglobulins), respiratorny failure, impaired swallowing, acute aspiration, secondary pneumonia

Prognosis- most have good QoL

Answer 73

A

Degeneration of dopaminergic neurones in the basal ganglia, particularly the substantia nigra

M2:F1, over 65 yrs

RF- genetic, enviromental factors (MPTP exposure- a drug that damages substantia nigra), drug-induced (anti-psychotics)

Answer 74

A

Parkinson’s Disease
A progressive brain disorder with movement and non-movement symptoms
Symptoms worsen slowly over time
Movement symptoms tend to improve with levodopa

Parkinsonism= Signs include slowness (bradykinesia), stiffness (rigidity) and resting tremor. parkinsonism symptoms progress quicker and often do not respond as well to levodopa.

Atypical Parkinsonism
A group of progressive brain disorders with some of the symptoms seen in PD
Symptoms are often more serious early on and progress quicker
Movement symptoms improve less or not at all with levodopa
1) Lewy Body dementia:
-memory loss
-visual hallucinations
-2) Progressive supranuclear palsy
- Postural instability/falls
- Impaired vertical gaze (hard to read or go down stairs)
- Cognitive impairment
3) Multisystem atrophy
- Postural hypotension- bp high when lay down
-Incontinence
-Impotence/ erectile dysfuncyion
4) Corticobasal syndrome
-jerky, involuntary movements
-loss of function on one side

Secondary Parkinsonism
Conditions that can look like PD, but are not always progressive
Symptoms may improve by treating the underlying cause
Movement symptoms usually do not improve with levodopa
- Drug induced parkinsonism (antipsychotics like haloperidol and anti sickness like metoclopramide) p- procyclidine for tremor
- brain tumours
- normal pressure hydrocephalus

Answer 75

A

1st - Urgent referral to neurology, medication can only be given by specialists

Durgs given aim to increase dopamine in substantia nigra

If motor symptoms affect quality of life
1st- levodopa or co-careldopa
- can have on-off effect
- nausea is side effect so give domperidone
- SE- dystonia, chorea and athetosis (involuntary writhing

If motor symptoms do not affect quality of life:
-Levodopa
-Dopamine agonists (ropinerole, pramipexole, apomorphine)SE= impulse disorders likepathological gambling
-MAO-B inhibitors (rasagiline) or COMT inhibitors (entacapone)
- All CRITICAL medicines and should not be stopped even on acute admission to hospital- need to be continuous to stop syptoms reoccuring

Vit D supplements

Physical therapy:
-Exercise
-Occupational therapy
-Speech therapy

AVOID ANTIPSYCHOTICS

Answer 76

A

COMP- dementia, constipation, depression, anxiety

PROG- progressive no cure

Answer 77

A

Bradykinesia - slowness of movement, shuffling gait, slow turning

Resting tremor- asymmetrical onset, improves with voluntary movement, pill-rolling, 3-5Hz

Rigidity- lead pipe (smooth risistance to passive movement of limb e.g elbow fexion) and cogwheel (jerky rigidity when passively flexing arm)

Postural Insability- imbalance or falling, festination (involuntary quickening), shuffling gait

TRAP- tremor, rigidity, achalasia, prostural instability

Other symptoms:
fatigue, constipation, depression, anxiety, insomia, hypomimia (reduced facial expression)

Answer 78

A

Diagnosis= clinical history and presenting features

Dopaminergic Agent Trial (DAT scan)- should improve symptoms

Single Proton Emission Computed Tomography (SPECT)

Answer 79

A

excess cerebrospinal fluid accumulates in the brain’s ventricles, but normal pressure

Answer 80

A

wet, wacky, wobbly

Urinary incontinence
Dementia
Gait abnormality similar to parkinsons

Neuroimaging- Ventriculomegaly without sulcal enlargement / or out of proportion to sulcal englargement

Answer 81

A

Result from systemic diseases (like diabetes and autoimmune disease) or localised damaged (trauma, compression, tumours) and manifest with neurological deficits distal to the level of the lesion

Cause
Injury - accidents can cut crush or compress nerves
Medical Conditions- diabetes, guillian-barre syndrome , carpal tunnel syndrome
Autoimmune Disease- SLE, RA, sjorens syndrome

Answer 82

A

Neuropraxia → compression injury causing temporary disruption of nerve conduction

Axonotmesis → axon is damaged but the perineurium and epineurium remain intact

Neurotmesis→ complete nerve transection

Traumatic Neuroma→ benign, painful nodular thickening caused by nerve regeneration at the site of different forms of nerve injury

Answer 83

A

immune mediated demyelination of peripheral nervous system usually a few weeks after injection (e.g campylobacter jejuni) get back/leg pain, progressive symmetrical weakness of all limbs starts in legs then reaches arms, absent reflexes

LP- rise in protein but normal WCC

Conduction velocity- decreased as demyelination

Answer 84

A

Compression of median nerve in carpal tunnel

Cause- pregnancy, oedema, RA

Symptoms- pins and needles in thumb, index and middle finger. weakness of thumb adduction, wasting of thenar eminance, Tinels sign (tapping causes parasthesia), Phalens sign (flexion of wrist causes symptoms)

Nerve conduction studies
EMG

Steroid injections, wrist splints at night
If severe- surgical decompression

Answer 85

A

Motor nerves: mucle weakness, painful cramps, uncontrollable muscle twitching

Sensory nerves: paraesthesia in hands and feet, trouble sensing pain or change in temp, walking

Autonomic nerves: excessive sweating, changes in bp, cant tolerate heat, GI symptoms

Answer 86

A

MEDIAN NERVE INJURY
- Wasting of thenar eminence
- Loss of sensation in lateral palmar surface of 3 and a half digits
- Weakness in abductor pollicis brevis
Median nerve usually effected by Carpal tunnel syndrome
Median nerve= C6-T1

ULNAR NERVE INJURIES
- Wasting of hypothenar eminence
- Loss of sensation over medial 1 and a half digits
- Weakness in abductor digiti minimi
- Claw hand
Ulnar nerve= C8-T1

RADIAL NERVE INJURIES
- Weakness of wrist extension → wrist drop
- Anaesthesia over first dorsal interosseous muscle
Radial nerve= C5-T1

KLUMPKE’S PALSY
- Paralysis of intrinsic muscles of hand
- Loss of sensation in ulnar distribution
- Horner’s syndrome sometimes present
Spinal cord level C8-T1

ERB’S PALSY
- Loss of shoulder abduction and elbow flexion
- Arm held internally rotated
- Waiter’s tip
Spinal cord level C5-C6

PEREONEAL NERVE INJURY
- Weakness in dorsiflexion and eversion of foot → foot drop
- Sensory loss over dorsum of foot
- Hit in side of knee
Spinal Cord Level L4-S1
L5 Radiculopathy would present with weakness of hip abduction and loss of inversion of foot

TIBIAL NERVE INJURY
- Inability to invert foot or stand on tiptoe
- Sensory loss on sole of foot
Spinal Cord Level L4-S3

Answer 87

A

Foot Drop ⇒ may be due to common peroneal nerve lesion (most common) or L5 radiculopathy. Common peroneal nerve lesion occurs due to compression at neck of fibula. Weakness of foot dorsiflexion and eversion. Weakness of hip abduction suggests L5 radiculopathy.

Answer 88

A

Plain X-ray or CT/MRI
EMG or Nerve Conduction Studies

Answer 89

A

1st line- conservative unless open injury
- Expectant management (allowing spontaneous recovery with close monitoring)
- Activity modification
- Splinting
- Electrical stimulation
- Physiotherapy
- Analgesia

Nerve repair or nerve transfer (if injury not healing properly on its own or if open injury)

Answer 90

A

MAIN SYMPTOMS
- Pain starting in area where spinal nerve roots are dysfunctional and radiates down to dermatome (shooting pain)

Motor- LMN symptoms for muscles innervated by this spinal root e.g. hyporeflexia
- Biceps ⇒ C5, C6
- Triceps ⇒ C7, C8 (Radial Nerve)
- Knee ⇒ L3, L4
- Ankle ⇒ S1, S2
  C5, C6 pick up the sticks. C7, C8 lay them straight.
  L3, L4 kick the door. S1, S2 buckle my shoe.
Sensory- dermatomal pattern of pain and numbness

Answer 91

A

Pinched nerve ROOT- condition where one or more nerves are affected and do not work properly
Happens when surrounding bone or tissue (cartilarge, muscles or tendons) put pressure on the nerve and disrupt its function
(neuropathy is issue with nerves, radiculopathy is issue with nerve roots)

CAUSE: mechanical compression of nerve root, intervertebral disk herniation, degenerative disc disease, osteoarthritis

Answer 92

A

CERVICAL RADICULOPATHY
Neck pain, headache, shoulder pain

C3/4 radiculopathy affects C2-C4 disks, shoulder and neck areas sensory deficits, scapular winging motor deficit
C5 radiculopathy affects C4-5 disks, affects sensation in anterior shoulder, affects bicep and deltoid movement, bicep reflex affected
C6 Radiculopathy affectc C5-6 disks, affects lateral side of elbow to thumb and lateral part of index finger, affects bicep and wrist extensors
C7 Radiculopathy affects C6-C7 disks, sensory deficity in middle finger and half of fingers 2 and 4, dorsal medial forearm. Affects movement of triceps, wrist flexors and finger extensors
C8 Radiculopathy affects C7-T1 disk. Sensation loss in half of 4th finger and pinky finger, hypothenar eminence and ulnar aspect of the distal forearm. Motor affects finger flexors, no reflex affected

Answer 93

A

Most common radiculopathy

Sciatica : compression of the sciatic nerve (lumbrosacral roots L4,L5,S1)

Cause: herniated intravertebral disk

Clinical Features: pain and tingling radiating from lower back to ipsilateral leg, weakness in calf muscles

Investigations: Straiht le raise test (pain on passive flexion of leg = lasegue’s sign)

Treatment: Physiotherapy, NSAIDs, if no improvement in 4-6 weeks then MRI

Answer 94

A

Lower back pain and leg pain, standing/sitting makes both worse. bending forward makes better as straightens the spine a bit

L5 specific symptoms = foot drop (weakness/paralysis of dorsiflexion and eversion of the foot), weakness of hip abduction and inversion of the foot, sesnosy loss over L5 dermatome, lower back pain that shoots down leg
Cause: Lumbosacral disk herniation, common pereoneal nerve lesion (compression at neck of fibula)

L3 radiculopathy affects L2-L3 disk, sensation impaired in anterior thigh (L2) medial thigh and over the knee (L3). Motor deficits in hip flexion, knee extension and hip adduction. Adductor reflex and patellar reflex affected

L4 radiculopathy affects L3-L4 disks. Sensory deficit in medial thight, area over patella(L3), medial aspect of leg , medial malleous(L4). Motor deficits in knee extension and hip adduction. Patellar reflex affected

L5 radiculopathy affects L4-5 disks. Sensory deficits in lateral aspect of thigh and knee, anterolateral aspect of the leg, dorsum of the foor and the big toe. Motor deficits in dorsiflexion of foot difficult heel walking as foot drop. big toe cant dorsiflex Posterior tibial reflex

S1 radiculopathy affects L5-S1 disks. Sensory deficit in the dorsolateral aspect of the thigh and leg and the lateral aspect of the foot. Motor cant evert foot and cant plantar flex foot (cant toe walk). Achilles reflex and latral hamstring impaired

S2/3/4 radiculopathy affects S1-4. Sensory deficit of posterior aspect of thigh and leg S2, perineum S3-4 and perianal S4. No motor issues. Bulbocavernous refex and perineal reflex affected

Answer 95

A

Positive straight leg raise test

EMG to assess nerve function

MRI spine if doesnt improve with conservative treatment

Answer 96

A

`conservative- NSAIDs, steroid injection, physiotherapy.

if symptoms dont improve in 4-6 weeks then MRI

Surgery if significant neurological defects

Answer 97

A

Lumbosacral nerve root compression at L4/5 or L5/S1.
Central disk prolapse

Lower back pain, bilateral sciatica, reduced perianal sensation, decreased anal tone, urinary dysfunction,

Urgernt MRI and surgical decompression

Answer 98

A

Brain and ventricles encased by skull so cant accomodate additional volume, if volume increases it leads to raised ICP

Causes:
-Idiopathic Intracranial hypertension: young overweight females
-CNS infection= meningitis
-Space occupying lesions= haemorrhage, tumours)
-Increased CSF= hydrocephalus
-cerebral oedema
-increased BP (malignany hypertension

Normal ICP= 15mmHg or less for adults in supine position

Answer 99

A

Cushing Triad- irregular breathing, widening pulse pressure, bradycardia = triad reflects brainstem compression

Bilateral Headache- worse in morning and after lying down. Worse when coughing/straining

Vomiting

Reduced consciousness

Bilateral visual loss (optic nerve compression-visual field testing)

Sixth nerve palsy

Papilloedema- (swelling of optic disk-see on fundoscopy)

Answer 100

A

CT Head (no contrast)/ MRI HEad

Intraventricular catheter (invasive)= motitoring put into ventricles with a CSF draining system, useful when CSF drainage is required for diagnostic and therapeutic reasons. ICP of over 20 indicates this is needed

Answer 101

A

If young, overweight female, Ct shows enlarged arachnoid outpouchings and prominent perivascular spaces and could be taking a tetracycline like doxycyline= weight loss and acetazolamide.

1st- Head elevation to 30 degrees

IV Mannitol (osmotic diuretic- hyperosmolar solution helping to draw water out the brain to reduce pressure

CSF Drainage if too much CSF through:
intraventricular catheter (hydrocephalus)
repeated lumbar puncture (e.g. idiopathic intracranial hypertension)
ventriculoperitoneal shunt (for hydrocephalus)

Controlled Hyperventialtion- reduced pCO2 which causes vasoconstriction of cerebral arteries= reduced ICP

Glucocorticoids- Dexamethosone, do if raised ICP is due to infection or inflammation like meningitis

Emergency Surgery- resection of tumour, haematoma evacuation

Answer 102

A

Cerebral oedema
Decreased cerebral perfusion pressure
Brain tissue herniation

Answer 103

A

An injury to the spinal cord resulting from processes that compress or displace arterial, venous, and cerebrospinal fluid spaces, as well as the cord itself

Causes:
Infection
Trauma- usually acute onset
Vertebral compression fractures (low energy trauma in pts with osteoporosis or osteomyelitis)- usually chronic onset
Vertebral metastasis (most common): from lung, breast, prostate, usually chronic onset
Intervertebral disk disease (herniation)- usually acute onset

16-30 yaers old- trauma most common
30-50 disk herniation
40-75+- malignancy

Answer 104

A

Lumbosacral nerve roots (L3-5) that extend below spinal cord are compressed

Cause Disc herniation (L4/L5 or L5/S1)

Decreased reflexes
Saddle anaesthesia
Faecal incontinence
Urinary incontinence
Bilateral sciatica
Decreased anal tone

Treat = Urgent MRI and then possible surgical decompression

Answer 105

A

Back pain → earliest and most common symptom, if its worse when lying down or coughing its a red flag for tumours or growths

Paraesthesia or numbness/sensory loss at level of lesion (LMN)

Weakness or paralysis bilaterally below affected level of spinal cord (UMN)

Bladder or bowel dysfunction- faecal incontinence and urinary retention

Hyperreflexia

See UMN signs below the level of the lesion and LMN signs at the level of the lesion

Answer 106

A

MRI Spine (whole spine)- look for disk displacement or mass, recommended within 24 hours of presentation

Answer 107

A

Depends on cause

1) Trauma spinal cord compression:
- Immobilisation
- Decompressive surgery
- IV corticosteroids (e.g. dexamethasone)

2) intervertebral disc compression (including cauda equina)
Decompressive laminectomy

3) Malignancy
High dose oral dexamethosone

Answer 108

A

COMP:
Pressure ulcers, UTI, DVT

Prog- depends on cause

Answer 109

A

An acute neurological condition resulting from a disruption in cerebral perfusion, lasting more than 24 hours

Ischaemic stroke (85%)
cerebral infarction due to insufficient blood flow due to a thrombus or embolus
Haemorrhagic stroke (15%)
cerebral infarction due to haemorrhage (rupture of blood vessel causing leakage of blood into the brain)

RF:
- Age >65
- Hypertension
- Diabetes
- AF
- Obesity
- Smoking
- High cholesterol

Answer 110

A

BAMFORD STROKE CLASSIFICATION

TACS (total anterior circulation stroke) vs PACS (partial anterior circulation stroke)
TACS is 3/3, PACD is 2/3
1) Unilateral weakness and/or sensory deficit of the face arm and leg
2)Homonymous hemianopia
3) Higher cerebral dysfunction (dysphagia, visuospatial disorder)

LACS (lacunar syndrome) one of the following
-pure sensory stroke
-pure motor stroke
-sensory-motor stroke
-ataxic hemiparesis

POCS (Posterior circulation syndrome) one of following:
-cranial nerve palsy and a contralateral motor/sensory deficit
- bilateral motor/sensory deficit
-conjugate eye movement disorder like gaze palsy
- cerebellar dysfunction- ataxia, nystagmus, vertigo
-isolated homonymous hemianopia or cortical blindness

Answer 111

A

All acute onset

MIDDLE CEREBRAL ARTERY
1) Contralateral weakness and sensory loss in upper limbs and lower half of face
2) Contralateral homonymous hemianopia
3) Aphasia:
- Broca’s area (left frontal lobe) causes Expressive aphasia → it’s responsible for speech production
- Wernicke’s area (left temporal lobe) causes Receptive aphasia → it’s responsible for speech comprehension

ANTERIOR CEREBRAL ARTERY
1) Contralateral weakness and sensory loss in lower limbs
2) Abulia (behaviour changes)
3) Urinary incontinence

POSTERIOR CEREBRAL ARTERY
1) Contralateral homonymous hemianopia with macular sparing
2) Visual agnosia (difficulty recognising familiar objects/faces)
3) Contralateral sensory loss
4) Memory deficits
5) Vertigo
6) Nausea
7) Stroke of midbrain branches of the posterior artery cause ipsilateral oculomotor palsy (down and out eye) and contralateral weakness of the upper and lower extremity

POSTERIOR CIRCULATION STROKE
1) Damage to the brainstem
2) Ipsilateral symptoms
3) Cerebellar signs (DANISH)
- Dysdiadochokinesia
- Ataxia
- Nystagmus
- Intention tremor
- Slurred speech
- Hypotonia
POSTERIOR INFERIOR CEREBELLAR ARTERY STROKE
Lateral medullary syndrome:
- cerebellar signs
- Nystagmus
- Vertigo and vomiting
- ipsilateral facial pain and temp loss
- contralateral upper and lower limb pain and temp loss
- ipsilateral Horner’s
ANTERIOR INFERIOR CEREBELLAR ARTERY STROKE
- Sudden onset vertigo and vomiting
- ipsilateral facial paralysis
- deafness

WEBER’S SYNDROME
A form of midbrain stroke characterised by:
- ipsilateral CN III palsy
- contralateral hemiparesis

PONTINE HAEMORRHAGE
- reduced GCS
- paralysis
- bilateral pin point pupils

BASILAR ARTERY STROKE
Locked in syndrome → decreased GCS and motor symptoms

POSTERIOR COMMUNICATING ARTERY ANNEURYSM
- 3rd nerve palsy (down and out eye, dilated pupil)
- Eye pain

Answer 112

A

Wernicke’s aphasia symptoms
- Speech fluent
- Comprehension abnormal
- Repetition impaired

Broca’s aphasia symptoms
- Speech non-fluent, laboured, and halting
- Comprehension normal
- Repetition impaired

Conduction aphasia symptom
- Speech fluent
- Comprehension normal
- Repetition impaired. Aware of the errors they are making

Global aphasia symptoms
- Speech non-fluent
- Comprehension impaired
- Repetition impaired

Speech non fluent ?
Comprehension intact= brocas
Comprhension not intact= global

Speech fluent?
Comprehension intact= conduction aphasia
Comprehension not intact= wernickes

Answer 113

A

ROSIER (Recognition of stroke in the emergency room) helps define between stroke and stroke mimics

Non-contrast CT-head: to exclude haemorrhage and confirm ischaemic stroke
CT angiogram: Look for which vessel is occluded

After patient been treated look for cause of stroke
- ECG to look for structural heard diseases
- Ambulatory ECG to look for atrial fibrillation
- Carotid doppler (if more than 70% occluded then do carotid endarteretomy to remove plaque)

Assess disability after a stroke using : Barthel index

Answer 114

A

1st- CT head before thrombolysis to rule out haemorrhage (esp if on warfarin/DOAC/has bleeding disorder)
- less than 4.5hours since onset= do thrombolysis (IV alteplase)
- for ACA within 6 hours do thrombectomy and thrombolysis (or for Posterior circulation over 24 hours)
(thrombolysis contraindicated if previous intercranial haemorrhage, seizure with onset of stroke, suspec subarachnoid haemorrhage, had stoke or traumatic brain injurt in last 3 month, pregnanct, actively bleeding, GI bleed in last 3 weeks, oesophageal varices, lumbar puncture in past week, intercranial neoplasm, uncontrolled hypertension above 200/120, INR over 1.7, hameorrhagic diathesis, active diabetic hameorrhagic retinopathy, major surgey in last 2 weeks, suspected intracardiac thrombus

if more than 4.5 hours
conservative management - 300mg oral aspirin with swallow assessment
after two weeks stop 300mg aspirin, start 75mg clopidogrel for life. If cant take clopidogrel then Apirin and modified release dipyridamole
if stroke was due to atrial fibrillation then : anticoagulation DOAC initiated 2 weeks after stroke

IF ipsilateral carotid artery stenosis over 70% then do carotid endarterectomy
- risk of hypoglossal nerve being damaged

IF hameorrhagic stroke patient
Stop anticoagulants (if on warfarin consider vitamin K and prothrombin concentrate,, also control BP if acute)

FOR TIA once haemorrhage rules out start anticoagulation immediately
If ischaemic stroke then start anticoagulation after 2 weeks

Answer 115

A

If think TIA: specialist and do MRI
if TIA or Stroke that have symptomatic carotid stenosis 50-99% NASCET or 70-99% ECST
- Referral urgently for carotid endarterectomy
- Blood pressure, anti platelet, cholesterol, lifestyle, diet

TIA or stroke pts who have symptomatic carotid artery stenosis less than 50% NASCE or less than 70 ECST
- Do not have surgery
- Blood pressure, anti platelet, cholesterol control, lifestyle

SUSPECT ACUTE STROKE
Non enhanced CT IMMEDIATELY IF
- Indication for thrombolysis or thrombectomy
- On anticoagulant
- Known bleeding issue
- GCS under 13
- Progressive or fluctuating symptoms
- Papilloedema, neck stiffness or fever
- Severe headache on onset of symptoms
If thrombectomy indicated: imaging with CT contrast angiography after this non enhanced CT
If thrombectomy indicated but after 6 hours: CT perfusion imaging

ACUTE ISCHAEMIC STROKE
THROMBOLYSIS (ATLEPLASE) IF:
- Within 4.5h since symptom onset
- Between 4.5-9h since symptom onset AND imaging shows potential to salvage tissue
- If woken with symptoms: Within 9h of midpoint of sleep AND potential to salvage tissue

(Assuming no contraindications, and haemorrhagic stroke excluded).

MECHANICAL THROMBECTOMY IF:
- Within 6h of symptom onset, with occlusion of proximal anterior circulation
- Between 6-24h of symptom onset/wellness, with occlusion of proximal anterior circulation AND potential to salvage brain tissue
- Within 24h of symptom onset/wellness, with occlusion of proximal posterior circulation (i.e. basilar / posterior cerebral atery) AND potential to salvage brain tissue

(Assuming adequate pre-stroke functional status).

If a person meets criteria for thrombolysis and mechanical thrombectomy, both can be given.

MOST IMPORTANT:
Within 4.5h, exclude haemorrhage, then give thrombolysis.
Within 6h, if proximal anterior circulation stroke, do mechanical thrombectomy.
(Add thrombolysis regardless if also meets under 4.5h criteria)

Beyond this, you need to do a CT perfusion / diffusion-weighted MRI scan to assess the potential to salvage brain tissue.

ASPIRIN AND ANTICOAGULATION
Aspirin 300mg orally or if have dysphagia then rectall. Continue for 2 weeks
If have AF or a clotting disorder don’t start aspirin until imaging confirmed
Prosthetic valve stop their treatment for a week and do aspirin

conservative management - 300mg oral aspirin with swallow assessment
- after two weeks stop 300mg aspirin, start 75mg clopidogrel for life. If cant take clopidogrel then Apirin and modified release dipyridamole
- if stroke was due to atrial fibrillation then : anticoagulation DOAC initiated 2 weeks after stroke instead of clopidogrel

Answer 116

A

Bleeding into the subarachnoid space (between arachnoid and pia) and is an emergency

Causes
- Traumatic SAH- head trauma
- Non-traumatic SAH = ruptured intracranial aneurysm (in circle of Willis then called berry aneurysm), arteriovenous malformations, anticoagulant use

RF:
- Age ≥50 y/o
- Smoking
- Alcohol
- Hypertension
- Family history of polycystic kidney disease (autosomal dominant)
- FH

Answer 117

A

Thunderclap Headache → severe, sudden-onset, occipital headache within 1-5 mins and lasts >1 hour
Reduced level of consciousness
Meningeal signs
- neck stiffness
- photophobia
- N&V
- seizures
- muscle aches

Answer 118

A

1st line - Non-contrast CT Head- diagnostic see hyperdense area in subarachnoid space → particularly in outline of circle of Willis and vasculature

If CT head is done less than 6 hours after symptom onset and is normal - dont lumbar puncture, may be something else

If CT is done after 6 hours and its normal - do lumbar puncture, Lp should be done 12 hours after onset to allow development of xanthochromia - biliirubin in CSF as RBC breaking down- the CSF sample will be yellow

If SAH is confirmed do CT angiogram to confirm location of bleed in vessel and the cause

Can do ECG to check for:
-arrhythmia
-prolonged QT (torsades de pointes)
- ST segment or T wave abnormalities

Electrolytes- Hyponatremia often found due to SIADH

Answer 119

A

Stop anticoagulants immediately

Nimodipine (calcium channel blocker) to prevent vasospasm as it can narrow blood vessel and block leading to ischaemia

Platinum endovascular coiling to treat intracranial aneurysms (clip it to stop bleeding)

Answer 120

A

COMP-
re-bleeding
vasospasm - delayed cerebral ischaemia
hyponatreamia SIADH
seizure
hydrocephalus

PROG- overall outcome is poor

Answer 121

A

Collection of blood between the dural and arachnoid coverings of the brain. Usually due to rupturing of bridging veins between the cortex and venous sinus.
As the volume of the hameorrhage increases the brain parenchyma is compressed and displaced and the ICP may rise and cause herniation

TYPES
1) Acute: less thna 3 days old, hyperdense bleed on imaging, normally trauma
2) Subacute: 4-20 days old with hyperdense bleed on imaging
3) Chronic: more than 20 days old, hypOdense bleed on imaging, usually from rupture of veins

RF
- Recent trauma
- Coagulopathy or anticoagulant use
- Alcohol use
- Advanced age >65 years old

Common demographic:
Males over 65

Answer 122

A

Can present several weeks after initial head injury
Gradual continuous headache → sign of raised ICP
Nausea/vomiting
Fluctuating confusion/consciousness or loss of consciousness
Diminished eye, verbal and motor response (low GCS)
Seizures
Lucid interval

Several weeks to month progressive history of either confusion, reduced consciousness or neurological deficit

Answer 123

A

Non contrast CT scan- See a cresent shaped bleed not limited by suture lines. If acute/subacute then hyperdense (white) bleed as its fresh blood, if chronic then hypodense as older (might be black cresent shaped). May cause a midline shift to contralateral side, crosses cranial sutures (aka not onfined by skull sutures) but does not cross midline

If CT inconclusive then MRI

Answer 124

A

Small- non complicated bleed:
-stop anticoagulants/antiplatelets
-start prophylactic antiepileptics (phenytoin or levetiracetam
-observe

Large bleed (over 10mm)
Acute → decompressive craniotomy
Chronic → burr hole evacuation

Chronic Bleed
-stop anticoagulants/antiplatelts
-start antiepileptics (phenytoin or levetiracetam)

Monitor ICP and try to reduce

Answer 125

A

COMP
-neurological deficity
-coma
-epilepsy

Prognosis →Acute SDH has a higher likelihood of an underlyingparenchymalinjury and is therefore associated with a worse prognosis than acute EDH. The prognosis of chronic SDH is better than that of acute SDH, however chronic SDH is associated with higher mortality with increasing age.

Answer 126

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Primary headache disorder → most common type of headache overall

Exacerbating factors
- Fatigue
- Lack of sleep
- Poor posture
- Anxiety
- Stress
- Depression
- Missing meals

Female 20-39 years old

Answer 127

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Episodic nature, lasts 30 mins to a couple of days
Band-like headache, often bilateral
May radiate to neck/shoulders
Dull, pressing, non-pulsating in character (lower intensity than migraines)
Relieved with painkillers
Headache doesn’t increase with exertion
No nausea, vomiting or aura (unlike migraines)

Answer 128

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Usually clinical diagnosis

Answer 129

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1st line : Aspirin, paracetomol, NSAIDs
prophylactic- amytriptyline or acupuncture

Lifestyle change
- Exercise
- Weight reduction
- Reduce mental tension

Answer 130

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COMP
peptic ulcers (due to NSAID use)

Prog- self treatment with analgesia usually effective

Answer 131

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Temporary, focal cerebral ischaemia that results in reversible neurological deficits without acute infarction that resolves completely with 24 hrs

Men and incidence increases with age

AF- most common
Valvular disease
Carotid stenosis
Congestive heart failure
Hypertension
DM
Smoking

Answer 132

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Sudden onset & brief duration of symptoms (most patients have resolution within 1 hour)
Unilateral weakness or paralysis
Dysphasia- indicates left sided ischaemia
Ataxia, vertigo or loss of balance- indicates posterior TIA
Homonymous hemianopia
Diplopia

Answer 133

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Urgent Carotid Doppler

CT head- if patient has bleeding disorder or is on anticoagulants to rule our haemorrhage

MRI brain with diffusion weighted imagine - to determine location

ECG- look for AF and rule out myocardial ischaemia

Bloods
-Blood glucose: exclude hypoglycaemia as the cause
- PT, INR, APTT: to exclude coagulopathy

ABCD2 score- estimate stroke risk

Answer 134

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GOLD STANDARD
Antiplatelet therapy - 300mg or clopidogrel for 2 weeks, after that 75mg clopidogrel for life
If already on anticoagulants do CT head to rule out haemorrhage
Treat BP only if only 220/120
If present within 7 days of episode= specialist review within 24 hours
If present after 7 days= specialist review within 7 days

Secondary long term prevention= Atorvastatin 80mg + antihypertensives

Carotid endarterectomy → carotid artery stenosis >70%

If atrial fibrillation give DOAC or Low Molecular Weight Heparin anticogulants

Cannot drive for 1 month

Answer 135

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COMP
stroke
myocardial infarction

Prognosis → no residual symptoms from the primary event. However, patients have increased risk of future ischaemic stroe

Answer 136

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A facial pain syndrome in the distribution of ≥1 divisions of the trigeminal nerve (Ophthalmic, Maxillary & Mandibular divisions). Caused by compression of the trigeminal nerve

Females, 60-70 years old

RF
increased age
multiple sclerosis

Associated with HSV

Answer 137

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Unilateral facial pain- severe sudden shooting stabbing (like electric shock) followed by burning ache. Lasts several seconds and may occur up to 100 times a day. Usually shoots from mouth to angle of jaw on affected side. Triggered by movements like chewing, talking or touch

Red Flag symptoms (refer to specialist)
- Sensory changes
- Deafness or other ear problems
- History of skin or oral lesions that could spread perineurally
- Pain only in the ophthalmic division of the trigeminal nerve (eye socket, forehead, and nose), or bilaterally
- Optic neuritis
- A family history of multiple sclerosis
- Age of onset before 40 years

Answer 138

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Clinical diagnosis

Answer 139

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Newly- Diagnosed- anticonvulsants (carbamazepine: this drug can cause SIADH and steven johnsons syndrome)

If dont respond to medical therapy refer to neurology to get microvascular decompression

Answer 140

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Acute, reversible condition caused by severe thiamine (vitamin B1) deficiency

Causes
- Chronic heavy alcohol use- most common
- Inadequate intake or malabsorption of thiamine
- Bariatric surgery predispose to thiamine malabsorption

M>F due to increased frequency of alcoholism in men

Answer 141

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Confusion
Eye sign:
- opthalmoplegia
-nystagmus, diplopia, ptosis
Gait ataxia- wide based takes small steps
Mental slowing, impaired concentration and apathy

COAT
- Confusion
- Oculomotor dysfunction (nystagmus + ophthalmoplegia)
- Ataxia
- Thiamine IV administration

Answer 142

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Korsakoff Syndrome (Wernicke’s is acute and reversible)

CART:
- Confabulation (making things up)
- Anterograde amnesia (cant create new memories)
- Retrograde amnesia (cant recall past)
- Temper altered

Answer 143

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Clinical diagnosis usually

Bloods: decreased thiamine
MRI - showing atrophy of mamillary bodies
Screening tools for alcohol withdrawal= CIWA Clinical Institute Withdrawal Assessment for Alcohol

Answer 144

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1st- immediate IV thiamine (pabrinex)
if patient just at risk and hasnt developed the condition then can supplement diet with thiamine

If delirium tremens and hallucinations- add a benzodiazepine like chlordiazepoxide

Abstinence from alcohol

Answer 145

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COMP:
ataxia
Korsakoffs psychosis
hearing loss
seizure

Prognosis- permanent brain injury if not treated early

Answer 146

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Homonymous hemianopia (loose both fields of same side, lesion is controlateral to which visual field lost)
- incongruous defects: lesion of optic tract
- congruous defects: lesion of optic radiation or occipital cortex
- macula sparing: lesion of occipital cortex

Homonymous quadrantanopias
- superior quadrantopia: lesion of the inferior optic radiations in the temporal lobe(Meyer’s loop)
- inferior quadrantopia: lesion of the superior optic radiations in the parietal lobe
- mnemonic = PITS (Parietal-Inferior, Temporal-Superior)
- Inferior and superior here refer to the quadrantanopia itself

Bitemporal hemianopia
- lesion of optic chiasm
- upper quadrant defect > lower quadrant defect = inferior chiasmal compression, commonly a pituitary tumour
- lower quadrant defect > upper quadrant defect = superior chiasmal compression, commonly a craniopharyngioma

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Neurological Conditions Flashcards

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