Neuro

Question 1

How common are brain tumours?

Answer 1

16th most common adult cancer, and 2nd most common children cancer

20/100000

Question 2

Presentation of a brain tumour?

Answer 2

symptoms of raise ICP: headache, reduced conscious level, nausea and vomiting

progressive neurological deficit and epilepsy

Question 3

Features of a raised ICP headache?

Answer 3

worst on waking from sleep, increased by coughing, straining and bending forwards, can be relieved by vomiting

Question 4

What is the cardinal physical sign or a brain tumour?

Answer 4

papilloedema

Question 5

What causes papilloedema?

Answer 5

obstruction of venous return from the retina

caused by loss of crisp optic nerve head margins, venous engorgement, retinal oedema, haemorrhages, raise ICP, intraneuronal ischemic damagee

Question 6

What types of focal neurological deficits are there?

Answer 6

motor, sensory, speech, visual, deafness, deteriorating memory, personality change

Question 7

What type of tumours are focal siezures more common in?

Answer 7

motor, sensory and temporal lobe

Question 8

Are primary or secondary brain tumours more common?

Answer 8

secondary

Question 9

Treatment of secondary brain tumours?

Answer 9

surgery, radiotherapy, chemotherapy, best supportive care

Question 10

When would surgery be considered for a brain tumour?

Answer 10

absent or controlled primary disease, younger than 75, good performance status

Question 11

Where is the main origin for primary brain tumours to occur from?

Answer 11

glial cells

Question 12

What is the main type of primary brain tumour?

Answer 12

astrocytoma (85-90%)

oligondendroglioma (5%)

Question 13

What is WHOs grading for gliomas?

Answer 13

1 - pilocytic astrocytoma (paediatric tumour)
2 - benign premalignant tumour
3 - anaplastic astrocytoma
4 - glioblastoma multiforme (THE MOST COMMON PHENOTYPE)

Question 14

If given enough time, what will all gliomas progress to?

Answer 14

glioblastoma multiforme (GBM) with the exception of pilocytic astrocytoma

Question 15

What is the common pathway to a malignant glioma?

Answer 15

initial genetic error in glucose glycolysis, mutation of isocitrate dehydrogenase 1 (IDH1), resulting in excessive build up of 2-hydroxyglutarate, triggering genetic instability in glial cells and subsequent inappropriate mitosis

Question 16

What is the less common pathway to a malignant glioma?

Answer 16

no IDH mutation, catastrophic genetic mutation, poor prognosis

Question 17

Survival of GBM?

Answer 17

20% survive more than 18 months, even with aggressive therapy

Question 18

Good prognostic factors for a glioblastoma?

Answer 18

under 50, aggressive surgical therapy, good performance post surgery, secondary GBM, MGMT mutatnt (as they means they should respond to chemo)

Question 19

Bad prognostic factors for a glioblastoma?

Answer 19

over 50, poor neurological function post surgery, non radical surgery treatment, primary GBM, MGMT wild type as means they wont respond to chemo

Question 20

Traditional vs updated glioblastoma therapy?

Answer 20

debulking surgery, radiotherapy

respective surgery, adjuvant chemo with temozolomide with RT, 6 cycles of teozolomide chemo

Question 21

How does temozolomide chemo treat brain tumours?

Answer 21

a prodrug, activated by HCl, crosses the blood brain barrier and then methylates guanine in DNA to make replication impossible at the base site

Question 22

Which tumour is resistant to Temozolomide?

Answer 22

MGMT, by reversing guanine methylation

Question 23

When does Temozolomide treatment work best?

Answer 23

any age, if debulk first, if performance status if low, no wild type MGMT

Question 24

What is WHOs performance status for any cancer patient?

Answer 24

1 - capable of light work
2 - self caring >50% of day
3 - limited self care

Question 25

How does avastin treat brain tumours?

Answer 25

it Is an anti angiogenic agent which shuts down the tumours blood supply

Question 26

Side effects of avastin?

Answer 26

hypertension, GI haemorrhage, expensive

Question 27

How does gene therapy treat brain tumours?

Answer 27

inoculation of tumour with replication deficient HSV-1 retrovirus so wild type HSV-1 replicates exponentially and causes encephalitis

modified HSV-1 fails to replicate in normal brain but replicates rapidly in GBM, causing oncolysis and release of progeny virus

tumour cells killed and normal brain cells unaffected

Question 28

How does dexamethasone treat brain tumours?

Answer 28

powerful synthetic steroid, given orally, improving brain performance, reduces tumour inflammation and oedema

Question 29

In who is a benign glioma commonly seen?

Answer 29

in the young, rare over 45

Question 30

What is the first symptoms of a benign glioma?

Answer 30

siezures

Question 31

What causes detioration in a benign glioma?

Answer 31

tumour transformation into a malignant phenotype, progressive mass effect due to slow tumour growth, progressive neurological deficit from destructional tumour

Question 32

Prognosis of an oligodenroglioma?

Answer 32

10-15yrs, can transform into anaplastic or GBM

Question 33

Treatment for oligodendroglioma?

Answer 33

chemotherapy

Question 34

What genetic deficits are in an oligodendroglioma?

Answer 34

chromosomes 1 and 19, IDH1 mutation positive

Question 35

What causes neurological deficit in brain tumours?

Answer 35

mass effect of tumour and surrounding cerebral oedema, deficit depends on tumour location

Question 36

What are the most common focal neurological signs seen from raised ICP in brain tumours?

Answer 36

3rd and 6th cranial palsy from stretching of the nerves by downward displacement of the temporal lobes

Question 37

DD of brain tumour?

Answer 37

intercranial mass lesions e.g. cerebral abscess, tuberculoma, subdural haematoma, intercranial haematoma, stroke, benign intracranial hypertension

Question 38

Investigations of a brain tumour?

Answer 38

imaging with CT and MRI, MR angiography, PET scan, CXR for metastases, avoid LP

Question 39

Risk factors of brain tumours?

Answer 39

ionising radiation, genetics, male, Africa, age

Question 40

What is MS?

Answer 40

multiple sclerosis - an autoimmune, inflammatory, demyelinating disease specific to the CNS which causes chronic neurological disability

Question 41

What is the mean onset of MS?

Answer 41

30 years

Question 42

Pathophysiology behind MS?

Answer 42

inflammation in white matter of the CNS, producing antibodies against EBV nuclear antigens which then attack CNS myelin due to molecular mimicry, causes demyelinations and axonal loss, causing MS plaques

Question 43

Risk factors for MS?

Answer 43

Caucasians due to less vit D, women, predisposition to EBV in children

Question 44

What is relapsing remitting MS?

Answer 44

random attacks over a number of years, mainly in first 3-4 years, recovery varies between patients and between attacks, disabilities accumulate with each attack

Question 45

What is chronic progressive MS?

Answer 45

slow decline in neurological functions either from the onset (primary) or following a relapse (secondary)

Question 46

What is benign MS?

Answer 46

few relapses and little disability

Question 47

Features of active MS?

Answer 47

demyelination (breakdown products present), variable oligodendrocyte loss, hypercellular plaque edge due to infiltration of tissue with inflammatory cells, perivenous inflammatory infiltrate, extensive blood brain barrier disruption, older active plaques have central gliosis

Question 48

Features of inactive MS?

Answer 48

demyelination (breakdown products absent), variable oligodendrocyte loss, hypocellular plaque, variable infllamtory infiltrate, moderate to minor blood brain barrier disruption, plaques gliosed

Question 49

Common sites and symptoms of MS?

Answer 49

cerebral hemispheres - large variety of symptoms

spinal cord - weakness, paraplegia, spasticity, tingling, numbeness Lhermitte’s sign, bladder, sexual dysfunction

optic nerves - impaired vision and eye pain

medulla and pons - dysarthria, double vision, vertigo, nystagmus

cerebellar white matter - dysarthria, nystagmus, intention tremor, ataxia

Question 50

Typical symptom of MS?

Answer 50

optic neuritis, spasticity, sensory symptoms and signs, Lhermittes sign, nystamus, double vision, vertigo, bladder and sexual dysfunction. gait

Question 51

Atypical symptoms of MS?

Answer 51

aphasia, hemianopia, extrapyramidal movement disturbance, severe muscle wasting, muscle fasciculation

Question 52

What are the first symptoms to present in MS?

Answer 52

weakness, parasthesiae and visual loss

Question 53

What is the essential diagnostic criteria for MS?

Answer 53

two or more CNS lesions, disseminated in time and space, exclude other clinical conditions

Question 54

Investigations for MS?

Answer 54

EP, MRI, CSF electrophoresis shows IgG oligoclonal bands, neurological examination, history, symptoms

Question 55

DD for MS?

Answer 55

SLE, autoimmune disease, lyme disease, syphilis, AIDS, adrenomyeloneuropathy, cardiac embolic event, mitchochondrial encephalopathy

Question 56

Treatment of MS?

Answer 56

IV methylprednisolone, SC B IFN

Question 57

side effects of B IFN?

Answer 57

injection site reaction, flu like symptoms complex, mild intermittent lymphopenia, mild to moderate rises in liver enzymes, flu like symptoms

Question 58

Treatment of spasticity in MS?

Answer 58

oral - baclofen, diazepam
peripheral never blocks e.g. phenol, alcohol, botox
intrathecal baclofen
functional neurosurgery
physio
remove trigger factors e.g. UTI, bed sores

Question 59

Treatment of tremor in MS?

Answer 59

BBs, low dose barbiturates, gabapentin, isoniazid, wrist bands containing small weights, computer controlled mechanical damping devices, stereotactic thalamotomy, thalamic electro stimulation

Question 60

Treatment of sexual dysfunction in MS?

Answer 60

sexual counselling, intracorporeal inhection of PGE, penile prosthesis, Viagra, vibrators, lubricating gels, local anaesthetics,

Question 61

Psychological effects of MS?

Answer 61

depression, anxiety, euphoria, pathological crying/laughing, cognitive dysfunction

Question 62

Characteristics of fatigue specific to MS?

Answer 62

fundamentally different from ordinary fatigue, exacerbating by heat, improved by cool temperatures, makes other symptoms appear worse

Question 63

The cause of pain in MS?

Answer 63

trigeminal neuralgia, painful tonic seizures, optic neuritis, vertebral compression fractures, ulnar and peroneal palsies, haemorrhagic cystitis, dysaesthic extremity pain, painful leg spasms, chronic joint and back pain

Question 64

Characteristics of paroxysmal symptoms in MS?

Answer 64

brief duration, occur frequently, triggered by various factors, positive symptoms, usually respond to anti convulsant therapy

Question 65

What is an impairment?

Answer 65

any loss of abnormality or psychological or anatomical structure or function

Question 66

What is a disability?

Answer 66

any restriction or lack of ability to perform and activity in manner or within normal range

Question 67

What is a handicap?

Answer 67

a disadvantage for a given individual resulting from an impairment or disability that limits or prevents the fulfilment of a role that is normal for that individual

Question 68

What is neurological rehabilitation?

Answer 68

restoration of the individual to the highest feasible functional level physically, psychologically, socially, economically with the constraints of impairemtns and disabilities and within the context of cultural mileu

Question 69

Wht is involved in MS physio?

Answer 69

special seating, moving ad handling techniques, passive stretching, standing and weight bearing, splints, serial casting

Question 70

How does GABAb baclofen treat spasticity?

Answer 70

reduces calcium influx, suppresses release of excitatory neurotransmitters and post synaptic increase in potassium conductance

Question 71

How does Tizanidine treat spasticity?

Answer 71

alpha2 agonist, peaks at 2 hours

Question 72

CI of Tizanidine?

Answer 72

hepatic impairments

Question 73

SE of Tizanidine?

Answer 73

dry mouth, hypotension, acute hepatitis, withdrawal, weakness

Question 74

How does dantrolene treat spasticity?

Answer 74

causes muscle relaxtion by interfering wuth calcium influx

Question 75

SE of dantrolene?

Answer 75

diarrhoea, avoid in liver disease

Question 76

How does Botox treat spasticity?

Answer 76

relatively localised hypertonia,

Question 77

How does THC (weed) treat MS?

Answer 77

CB1 presynaptic receptors inhibit calcium influx, inhibits glutamate release and activates potassium channels

Question 78

What causes gait in MS?

Answer 78

weakness, foot drop, sensory ataxia, cerebellar ataxia, spasticity, drug side effects, fatigue

Question 79

Treatment of gait in MS?

Answer 79

treat cause, physio, fall education, walking stick, orhoptics, functional electrical stimulation, famipridine, botox

Question 80

How does dalfampridine treat MS?

Answer 80

prevents back propagation of action potentials, inhibits postassium channels so there is better conduction along demyelinated axons

Question 81

What does detrusor overactivity cause?

Answer 81

frequency, urgency, incontinence

Question 82

What does detrusor areflexia cause?

Answer 82

flaccid, large bladder

Question 83

What does detrusor sphincter dysnergia cause?

Answer 83

incomplete bladder emptying

Question 84

What does sphincter over activity cause?

Answer 84

retention and hesitancy

Question 85

What does sphincter incompetence cause?

Answer 85

dribbling

Question 86

What is the diagnosis criteria called for MS?

Answer 86

McDonalds criteria

Question 87

Which nerves are never affecting in MS?

Answer 87

peripheral

Question 88

What percent of strokes are caused by intracerebral haemorrhages

Answer 88

10-15%

Question 89

How does an intracerebral haemorrhage present?

Answer 89

sudden onset headache, drowsiness, vomiting, focal deficit

Question 90

What is dementia?

Answer 90

describing symptoms of poor memory and difficulty learning

Question 91

What causes dementia?

Answer 91

damage to brain cells, the most common cause being Alzheimer’s

Question 92

What is Alzheimer’s?

Answer 92

a neurodegenerative disease, mainly in the cortex, causing plaques and tangles, leading to dementia

Question 93

What does the Amyloid Precursor Protein do?

Answer 93

helps neurons in the brain grow and repair itself after an injury

Question 94

What enzyme breaks down the APP and what does this lead to?

Answer 94

alpha-secretase and gamma-secretase, and the broken up protein parts are soluble and go away

Question 95

What happens when beta-secretase and gamma-secretase breaks down APP and what does this lead to?

Answer 95

the left over fragment is not soluble and forms the monomer amyloid beta which are chemically sticky and bind together outside the neurons, leading to beta amyloid plaques which can get between neurons and inhibit neuron signalling so memory is impaired and can cause an autoimmune response, damaging surrounding neurons, can also deposit around blood vessels, lead to amyloid angiopathy, increasing risk of haemorrhage, rupture and blood loss

Question 96

What 3 things can amyloid beta lead to in Alzheimer’s?

Answer 96

beta amyloid plaques, autoimmune inflammation and amyloid angiopathy

Question 97

What are tangles in Alzheimer’s?

Answer 97

found inside the cell

Question 98

What protein holds together neurons in the brain?

Answer 98

tau protein

Question 99

What effect do beta amyloid plaques have

Answer 99

inhibit neuron signally and initiates activation of kinase in the neurons, which transfer phosphate groups to the tau protein so it changes shape and then the tau protein can no longer support the microtubules, clumps together with other tau proteins and gets tangled, leading to neruofibrially tangles

Question 100

What do neurofibrially tangles lead to in Alzheimer’s?

Answer 100

signals cannot be passed along the neurons in the brain and can lead to apoptosis leading to brain atrophy, narrow gyri, wider sulci and larger ventricles in brain

Question 101

What are the two types of Alzheimer’s?

Answer 101

sporadic and familial

Question 102

What is sporadic Alzheimer’s?

Answer 102

late onset, unknown cause, due to genetic and enviromental risk factors, the most common time, risk increased with age, linked to e3 allele of apolipoprotein E gene (APOE-e4), the risk increases if more of these genes were inherited

Question 103

How common is sporadic Alzheimer’s?

Answer 103

most common Alzheimer’s

1% age 60-65
50% age 85

Question 104

Function of apolipoprotein E?

Answer 104

breaks down beta amyloid

Question 105

Why does APOE-e4 genes develop Alzheimer’s?

Answer 105

the gene is less effective at breaking down beta amyloid, leading to increased plaques

Question 106

What is familial Alzheimer’s?

Answer 106

dominant gene speeds up progression, early onset, caused by

gene mutations in PSEN1 (c14) or PSEN2 (c1) gene   are linked as they encode for presenilin 1 and 2 which are subunits of gamma secretase, so will change the location of APP splitting, increasing beta amyloid
OR
Trisomy 21 (Downs) which has an extra copy of c21 which codes for APP gene which increase amyloid plaque build up

Question 107

Symptoms of Alzheimer’s?

Answer 107

can be undetectable in early stages then leads to short term memory, loss of motor skills, language is affected, then lose long term memory, until more disorientated and bedridden

Question 108

What is the most common cause of death in Alzheimer’s?

Answer 108

infection e.g. pneumonia

Question 109

How do you diagnose Alzheimer’s?

Answer 109

brain biopsy (after death) so must just exclude other causes of dementia for diagnosis

Question 110

Treatment of Alzheimer’s?

Answer 110

no cure, few medications which help and none that hault progression

Question 111

Functions of the frontal lobe?

Answer 111

voluntary and planned motor behaviours, motor speech area, personality, planning

Question 112

What happens in fronto temporal dementia?

Answer 112

personality and behaviour change followed by breakdown in attention and executive function (behavioural variant FTD)

Question 113

Function of the temporal lobe?

Answer 113

hearing, language, semantic knowledge, memory, emotional/effective behaviour

Question 114

What is HM amnesic?

Answer 114

severe epilepsy, profound failure to create new memories

Question 115

Treatment of HM amnesic?

Answer 115

surgery to bilateral to remove medial temporal lobes including hippocampus

Question 116

What is preclinical Alzheimer’s?

Answer 116

amnesic prodrome which memory impairment, poor performance on episodic memory tests, cognitive function is preserved, scored on cognitive/memory screening, high risk of developing Alzheimer’s

Question 117

What is used to assess cognitive function?

Answer 117

6CIT

Question 118

What is involved in the 6CIT?

Answer 118

what year is it?
what month is it?
give an address with 5 parts?
count down from 20
say months of year in reverse
repeat address

Question 119

definition of functional memory disorder?

Answer 119

acquired
>6 months
affect personal/professional life
psychosocial burden/psychological distress
verbal memory and attentional capacity >-1.5SD
absence of organic cause of cognitive memory
absence of major psychiatric disease (severe depression)

Question 120

What is the criteria called for Alzheimer’s?

Answer 120

consensus criteria Braak
1/2 = low likelihood
3/4 = intermediate likelihood
5/6 = high likelihood

diagnosis in intermediate of high likelihood of Alzheimer’s are met and patient has clinical history of dementia

Question 121

What condition is Alzheimer’s linked to?

Answer 121

parkinson’s disease

Question 122

Investigations for Alzheimer’s?

Answer 122

PET and SPECT, functional MRI

Question 123

Management of Alzheimer’s?

Answer 123

prevention, support, carers, advice, medications, socially active, cognitively active, control vascular risk factors, treat mood and anxiety

Question 124

What are Caerphilly healthy behaviours for Alzheimer’s?

Answer 124

no smoking, BMI 18-25, 3 or more portions of fruit/veg, and less than 30% of calories from fat, walking 2 or more miles each day, or vigorous exercise as a regular habit,

Question 125

What medications can be used for Alzheimer’s?

Answer 125

AtCh esterase inhibitors e.g. exelon, aricept, reminyl or memanrine (anti glutamate) or NMDA receptor antagonists e.g. namenda

Question 126

Screening and staging instruments for mental status?

Answer 126

MMSE, mental state questionnaire, clinical dementia rating, global deterioration scale, ACE-R, CERAD, CAMDEX, ADAScog, MoCA

Question 127

What are the 5 diffferent cognitive areas in the MMSE?

Answer 127

orientation, memory, attention, language, visual processing

Question 128

What tests and questions are used for Alzheimer’s testing?

Answer 128

address, date, birth, priminister, clock drawing test, fluency test or letters and design, how many animals can you name in one minute, card sorting test, stroop test, visualspatial memory and visuocontructive abilities, constructional apraxia, closing in phenomenon, £D visuoconstructive abilities, non verbal intelligence, abstract reasoning, verbal comprehension, spontaneous speech

Question 129

What preventitive drugs can be used for Alzheimer’s?

Answer 129

manage vascular risk, statins, antioxidants, anti inflammatory drugs, oestrogen, social interventions

Question 130

What is epilepsy?

Answer 130

recurring, unpredictable siezures

Question 131

What is a seizure?

Answer 131

when neurons are synchronously active in the brain, it is a paroxysmal event which changes behaviours, sensations and cognitive behaviour, caused by an abnormal burst of electrical impulses or too little inhibition

Question 132

What happens in epilepsy with too much excitation?

Answer 132

fast of long lasting activation of NMDA which causes calcium to come in

Question 133

What happens in epilepsy with too little inhibition?

Answer 133

There is too little GABA receptors so cannot inhibit signals

Question 134

Potentially causes of epilesy?

Answer 134

primary, or secondary to tumours, brain injury and infection

Question 135

What are common outward signs seen in epilepsy?

Answer 135

jerking (typically beginning in corner of mouth and thumb and spreading to the limbs), moving, losing consciousness, starts on one side and then moves to the other, can be followed by a period of complete paralysis

Question 136

What are common inward symptoms seen in epilepsy?

Answer 136

fears, strange smells

Question 137

What are the 2 types of seizures?

Answer 137

generalized or focal/partial - depends on how much of the brain is affected

Question 138

What are the two types of partial seizure?

Answer 138

simple and complex

Question 139

What happens in a simple parital seizure?

Answer 139

affects small part of brain
remain conscious
strange sensations and jerking movements
can be a warning that another seizure is coming
be aware that something is happening
remember the seizure
sense of deja vu

Question 140

What is a Jacksonian march?

Answer 140

when movements start in on e group of muscles and spreads to other groups

Question 141

What happens in a complex partial seizure?

Answer 141

impaired consciousness/impaired awareness
unresponsive
may not remember
may just be small movements e.g. smacking lips, rubbing hands, moving arms

Question 142

What is Todd’s paralysis?

Answer 142

the paralysis post seizure

Question 143

DD for blackouts?

Answer 143

syncope, non epileptic seizure, epilepsy

Question 144

What is a generalized seizure?

Answer 144

When both hemispheres are affected (secondary if starts as a partial seizure)

Question 145

What is a tonic seizure?

Answer 145

muscles become stiff and flex, can lead to a fall backwards

Question 146

What is an atonic seizure?

Answer 146

muscles become relaxed and can lead to a forward fall

Question 147

What is a colonic seizure?

Answer 147

violent muscle contractions (convulsions)

Question 148

What are tonic-clonic seizures?

Answer 148

most common generalized seizure, have a tense phase when the patient stiffens up and then the muscles start to rapidly contract

Question 149

What are myoclonic seizures?

Answer 149

short muscle twitches, can be just a single twitch or can be lots

Question 150

What are absence seizures?

Answer 150

patient loses consciousness and then quickly regains it, the patient may just look spaced out

Question 151

What is status eplilepticus?

Answer 151

seizure >5 mins, or multiple seizures without returning to normal

normally tonic clonic type seizure

medical emergency

Question 152

Treatment of status epilepticus?

Answer 152

acutely with benzodiazepines, o2, cardiorespiratory monitoring, vitamins IV

Question 153

How do benzodiazepines treat epilepsy?

Answer 153

enhance effect of the inhibitor GABA

Question 154

What symptoms follow seizures?

Answer 154

confusion (post ictal confusion), paralysis of arms and legs (normally on one side but can last up to 15 hours - Todds paralysis)

Question 155

What causes Todd’s paralysis?

Answer 155

temporary severe suppression of activity in the brain which was affected by the seziure

Question 156

What investigations are done in epilepsy?

Answer 156

MRI, CT, EEG - to find anatomical abnormalities

evaluation of seizure and eye witness accoutns

Question 157

Function of EEG?

Answer 157

detects electrical activity in the brain

Question 158

Treatment of epilepsy?

Answer 158

anti convulsants based on the patient

epilepsy surgery if small part of the brain can be removed

nerve stimulation influences vagus nerve to influence neurotransmitter release to reduce frequency and severity of seizures

ketogenic diet so body burns fat not carbohydrates which produces ketone bodies which are used as an energy source by the brain instead of glucose

stress relievers, avoid triggers, avoid contact sports and swimming, and must be seizure free for a year to drive

deep brain stimulation implants electrode into specific areas of the brain, reducing abnormal electricity, reducing frequency of seizures

Question 159

Who do absence seizures commonly affect?

Answer 159

children, can appear as a stop in conversation or daydream

Question 160

How long do complex partial seizures last for?

Answer 160

around 2-3 minutes

Question 161

Triggers of epilepsy?

Answer 161

flashing lights, CV disease, cerebral tumours, alcohol, post trauma, genetics

Question 162

What anti epileptic drugs are used for focal seizures?

Answer 162

Lamotrigine and Carbamarzepine

pre synaptic and stop excitary signals

Question 163

What anti epileptics drugs are used for generalized seizures?

Answer 163

lamotrigine and sodium valproate

Question 164

Side effects of anti epileptic drugs?

Answer 164

memory problems, hepatic enzyme inhibition, weight gain, hair loss, rashes, leucopaenia

Question 165

What is the dosage of anti epileptic drugs?

Answer 165

start low and gradually build up, until seizures stop or until you develop side effects, aim to achieve control with minimum dosage, and there is risk of intoxication which can lead to ataxia, nystagmus and dysarthria

Question 166

When should to do surgery for epilepsy?

Answer 166

when only a single part of the brain is causing the seizures and it can be removed without causing any significant loss of brain function

Question 167

Side effects of anti epileptic drugs?

Answer 167

it is a shock every 5 minutes for 30 seconds, hoarseness, sore throat and cough

Question 168

Symptoms of non epileptic seizures?

Answer 168

pelvic thrusting, no tongue biting, eyes closed, crying/speaking, change in amplitude not frequency of activity

Question 169

Side effects of DBS?

Answer 169

bleeding on the brain, depression, memory problems

Question 170

What cause a non epileptic seizure?

Answer 170

mental process caused by psychosocial distress, and seizure instead of the emotion, it is situational and can last 1-20 minutes

Question 171

What causes syncope?

Answer 171

fainting, changing behaviour sensation and cognitive processes, causing by insufficient blood of O2, from standing or sitting, lasting 5-30 seconds, has less warning and a history of heart disease

Question 172

What is parkinsonism?

Answer 172

a triad of symptoms of tremor, rigidity/increased tone and bradykinseia

Question 173

How common is Parkinson’s?

Answer 173

0. 3% of population over 40
1. 5 million worldwide

more common in men

most common at 65

Question 174

Sign and symptoms of Parkinson’s?

Answer 174

tremors, rigidity, bradykinesia, postural instability

hypominia, dysphagia, hypophonia, blurred vision, eyelid opening apraxia, gait (shuffling, freezing)

reduced smell, constipation, visual hallucinations, frequency, urgency, dribbling of saliva, depression, dementia

Question 175

What part of the brain is mainly affected in Parkinson’s?

Answer 175

basal ganglia - which is responsible for muscle tone and ease of movemt

Question 176

What makes up the basal ganglia?

Answer 176

caudate nucleus, caudate putamen, globus pallidus (interna and externa), nucleus accumbens, subthalamic nuclei, substantia nigra (2 parts)

Question 177

Function of the basal ganglia?

Answer 177

cerebral cortex sends signals to the basal ganglia to initiate movement. The basal ganglia will control skeletal muscle tone and coordination of learned movements and then it will send signals back to the cortex (motor) via the thalamus to then be initiated down the spinal cord, out of the ventral horn to have normal movement pattern

Question 178

How is the basal ganglia affected in Parkinson’s?

Answer 178

problem with the output, so no normal controlled movement pattern

Question 179

Function of substantia nigra?

Answer 179

has dopamine neurogic neurons which release dopamine into the striatum which then binds to dopamine 1 or 2 (excitory or inhibitory)

Question 180

Pathophysiology of Parkinson’s?

Answer 180

reduced dopamine in the substantia nigra leading to apoptosis or necrosis of dopaminergic neurons

caused by protein misfolding, aggregation and toxicity, defective proteolysis, mitchondrial dysfunction, oxidative stress

demyelinataion, neuronal loss and glyosis in substantia nigra, presence of Lewy bodies

lack of dopamine mean it cannot bind to GABA neuron so the inhibitory GABA is overstimulated causing glutamate secretion, causes excessive inhibitor input to the thalamus causing suppression of thalamocorticospinal pathway, so movement is not smooth

Question 181

What are Lewy bodies?

Answer 181

round eosinophilic intra cytoplasmic occlusions in the nuclei of neruone, made up mainly of alpha-synciclein ubiquitin and other proteins

Question 182

Risk factors of Parkinson’s?

Answer 182

familial, GBA, CNCA, LRRK2, PARK2 and PINK1, pesticides, survivors of the encephalitis lethargica

Question 183

Protective factors of Parkinson’s?

Answer 183

smoking, coffee, vigorous exercising, NSAIDs

Question 184

Treatment of Parkinson’s?

Answer 184

Levodopa, dopamine agonists, monoamine oxidase B inhibitors, catechol-o-methyltransferase inhibitors, BBs, antichloinergics, physio, dietitian, language therapist, specialist nurse, counselling, surgery, DBS

Question 185

How does levo-dopa treat Parkinson’s?

Answer 185

it is a precursor to dopamine to improve symptoms

Question 186

What does levo dopa need to be prescribed with and why?

Answer 186

a peripheral dopadecarboyxlase inhibitor e.g. benserazide to prevent it being converted to dopamine too early in the bloodstream, and reduces it peripheral side effects (nausea and compulsive behaviours)

Question 187

How do dopamine agonists treat Parkinson’s and what are the side effects?

Answer 187

act as a dopamine agonist and do not need to be converted in the body to become active, but risk of impulsive control disorders and excessive sleepiness

Question 188

How do MAO-B inhibitors treat Parkinson’s?

Answer 188

e.g. selegiline and rasagiline inhibit levodopa and dopamine breakdown so the effects last longer

Question 189

How do COMT inhibitors treat Parkinson’s?

Answer 189

prevent levodopa breakdown, so more of the dose can reach the brain

Question 190

What is a myasthenia gravis?

Answer 190

chronic, acquired, autoimmune neuromuscular disease

Question 191

Pathophysiology of myasthenia gravis?

Answer 191

autoantiboies to acetylcholine receptors (anti-AChR antibodies) at the post synaptic membrane, causing depletion of working post synaptic receptor sites and interfering with the neuromuscular junction

associated with HLAB8 and DR3, or induced by drugs e.g. penicillin

Question 192

When does myasthenia gravis occur?

Answer 192

most common in young women under 40 and old men over 60

can be passed onto neonates

15/100,000 but is underdiagnosed

Question 193

What diseases is myasthenia gravis associated with?

Answer 193

other autoimmune disease, thymic atrophy, tumour of SLE

Question 194

Signs and symptoms of myasthenia gravis?

Answer 194

drooping eye, slurred speech, difficulty breathing, blurred/double vision, weakness in arms and legs, change in facial expression, unable to hold a steady gaze, difficulty chewing, weakness in proximal muscles, affect diaphram and resp troubles

Question 195

What exacerbates and relieves myasthenia gravis?

Answer 195

exacerbated in exercise but relieved by rest

Question 196

Causes of myasthenia gravis?

Answer 196

bone marrow transplant, or IFN-a medication,

Question 197

Why is the thymus large at birth?

Answer 197

as it is responsible for immune response and the immune system is low at birth, it decreases in size as we get older

Question 198

What size is the thymus in myasthenia gravis?

Answer 198

abnormal and large, can people can develop thymoma,

Question 199

Investigations for myasthenia gravis?

Answer 199

examine eyes and muscles for signs of weakness
anti AChR positive or anti MuSK positive
CT and MRI look for thymoma
nerve conduction measured - fatigue will occur quicker in myasthenia gravis
single fibre EMG measure elecrtical potential form nerve to muscle, lower in myasthenia gravis
ice test, crushed ice in glove over eye for 3 minutes, which leads to imporved ptosis in myasthenia gravis

Question 200

Treatment of myasthenia gravis?

Answer 200

increase sleep, avoid stress and excessive heat, rest, immunosuppressants e.g. prednisolone, acetylcholinesterae inhibitors inhibitors for temporary symptomatic relief by increasing ACh availiability (but beware of cholinergic crisis), osetoporosis prophylaxis, modified diet if difficultuy swallowing, thymectomy

Question 201

What is myasthenia gravis cholinergic crisis?

Answer 201

weakness of the respiratory muscles during a relapse which is life threatening

Question 202

Treatment of myasthenia gravis cholinergic crisis?

Answer 202

monitor FVC, ventillatory support, plasmapheresis, IV Ig, identify triggers and treat them

Question 203

Prognosis of myasthenia gravis?

Answer 203

5% mortality with treatment
25-30% without treatment

inter current infection and hot weather aggravate it

Question 204

What is Guillain Barre syndrome?

Answer 204

acute inflammtory demyelinating and occasional axonal polynaruopathy

Question 205

Causes of Guillain Barre syndrome?

Answer 205

infection leading to shared epitopes with an antigen in the peripheral nerve tissue (ganglioside GM1 and GQ1b) leading to an autoantibody mediated nerve cell damage

Question 206

triggers of Guillain Barre syndrome?

Answer 206

infection with campylobacter jejuni, EBVm CMV, post pregnancy (risk decreases during pregnancy), malignancies, vaccines

Question 207

How common is Guillain Barre syndrome?

Answer 207

1/100,000 a year, everyone equally likely to get it, but more men than female had it and peak ages are 15-35 and 50-75

Question 208

What is the first symptom in Guillain Barre syndrome?

Answer 208

paraesthesia and sensory loss in lower extremities

Question 209

Symptoms of Guillain Barre syndrome?

Answer 209

ascending symmetrical weakness, neuropathic pain in legs and pain, reduced or absent reflexes early, reduced sweating, reduced heat tolerance, bladder weakness, postural hypertension, cardiac arrhythmias, urinary hesitancy

Question 210

Complications of Guillain Barre syndrome?

Answer 210

can lead to paralysis, and can be severe if respiratory and facial muscles are involved which can cause respiratory fialure, hypo/hypertension, cardiac arrhythmia, urinary retention, ileus, pneumonia

Question 211

DD for Guillain Barre syndrome?

Answer 211

stroke, brianstem compression, cord compression, poliomyelitis, myasthanthia gravis, hypokalaemia, vasculitis, botulism, encephalitis

Question 212

Investigations for Guillain Barre syndrome?

Answer 212

high ADH secretion
LP - increased CSF protein
antibodies present
nerve conduction studies
ECG
MRI to exclude other causes

Question 213

Management of Guillain Barre syndrome?

Answer 213

plasma exchange, IV Ig, corticosteroids, DVT prophylaxis, ITU for ventilation and intubation, pain relied, physio, nasogastirc feeding if swallowing problems, counselling

Question 214

Prognosis of Guillain Barre syndrome?

Answer 214

good, but 10% die from resp failure, pulmonary emboli, infection or prolonged paralysis

poorer prognosis if old, rapid progression of symptoms, prolonged ventilation, preceding diarrhea, muscle dysfuction

Question 215

What is the Miller Fisher syndrome?

Answer 215

variant of Guillain Barre syndrome that affects cranial nerves to the eye muscles and presents with opthamoplegia and ataxia

Question 216

What are the different subtypes of Guillain Barre syndrome?

Answer 216

AIDP (95%)
AMSAN (GM1, GM1b and GD1a)
AMAM
ASN
acute pandysautomina

Question 217

What is giant cell arteritis?

Answer 217

aka temporal arteritis - granulomatous arteritis with inflammed medium and large arteries leading to occlusion o the lumen leading to ischemia of the optic nerve

Question 218

In who does giant cell arteritis occur?

Answer 218

over 60s, related to polymyalgia rheumatic in 50% of cases

Question 219

Symptoms of giant cell arteritis?

Answer 219

fever, fatigue, headache, SCALP PAIN, headache in front or on temples, JAW PAIN and claudication, diplopia, ptosis, blurred vision, amaurosis fugax, symptoms develop quickly, tenderness of temporal artery

Question 220

What are the specific symptoms for giant cell arteritis?

Answer 220

jaw claudication and pain, scalp pain

Question 221

Diagnosis of giant cell arteritis?

Answer 221

biopsy of temporal artery to confirm with GRANULOMATOUS CHANGES, elevated inflammatory markers, increased platelets and alkaline phosphate, decreased Hb, normonchromic, normocytic anaemia

Question 222

Treatment of giant cell arteritis?

Answer 222

prednisolone immediately during biopsy, high dose methylprednisolone injection then prednisolone tablets, start high dose and then decrease, low dose aspirin, PPI to protect against stomach ulcers, immunosuppressants during prednisolone reduction, gastric and bone protection

Question 223

Complications of giant cell arteritis?

Answer 223

irreversible bilateral visual loss, CV disease

Question 224

What trigeminal neuralgia?

Answer 224

paroxysm of intense, sudden, stabbing pain in trigeminal never distribution from compression of the trigeminal nerve where it enters the brainstem, this pressure wears away at the myelin sheath causing uncontrollable pain

Question 225

Symptoms of trigeminal neuralgia?

Answer 225

intense, sharp jabbing pain in forehead, cheek or jaw, dental pain, pain on one side of the face

Question 226

Causes of trigeminal neuralgia?

Answer 226

MS, tumours on the nerve, compression of the nerve by a small artery or vein as it leaves the brain stem

Question 227

What are the 3 branches of the trigeminal nerve and which is the least common to get trigeminal neuralgia?

Answer 227

mandibular, maxially and opthalamic (least common)

the pain is usually in 1 or 2 of the divisions

Question 228

Triggers of trigeminal neuralgia?

Answer 228

washing the affected area, shaving, eating, talking, dentist, kissing, cold breeze, head movement, vibrations, hot or cold food, caffeine

Question 229

DD of trigeminal neuralgia?

Answer 229

root canals

Question 230

Investigations in trigeminal neuralgia?

Answer 230

rule out other conditions with MRI and history

Question 231

Treatment of trigeminal neuralgia?

Answer 231

anticonvulsants e.g.carbamazipine to relieve nerve pain and slow down electrical impulses in the nerves and reducing the ability to transmit pain, it becomes less effective over time

gabapentin, phenytoin

thermocoagulation of the trigeminal ganglion or section of the sensory division

microvascular decompression to seoarate vessels from nerve root

stereotactic knife surgery - effective but has complications of facial numbness, hearing loss, stroke and death

injection of glycerol into the nerve

Question 232

Side effects of carbamazipine?

Answer 232

tiredness, dizziness, confusion, nausea, double vision, leukopenia, depression

Question 233

What is anesthesia dolorosa?

Answer 233

rare combination of numbeness and continuous pain in trigeminal neuralgia, it is virtually untreatable

Question 234

What is the ganglion called where all 3 trigeminal nerve branches meet?

Answer 234

Gasserian ganglion

Question 235

What is Huntington’s disease?

Answer 235

neurodegenerative disease cauign atrophy and neruonal loss of striatum and cortex, leading to depletion in GABA and ACh, also increasing lenght of CAG triplet

Question 236

What is the huntington gene and what chromosome is it on?

Answer 236

a increased in length of a cysteine-adenosine-guanine triplet repeat in the huntington gene on c4, the longer the repeat the earlier the onset of the disease

Question 237

How common is Huntington’s disease?

Answer 237

1/10,000, it is familial, autosomal dominant, 50:50 change of passing it on

Question 238

Symptoms of Huntington’s disease?

Answer 238

clumpsy, restless, muscle twitches and spasms, become more difficult to perform tasks, CHOREA

poor communications and starting conversations and undersatnd

poor attention spam and memory

depression, apathy, change in sexual behavior, anxiety, aggressive,

Question 239

When does Huntington’s disease usually present?

Answer 239

30-60years, 6% are juvinile though, people die 10-20 years after diagnosis

Question 240

Pathophysiology of Huntington’s disease and the 3 types?

Answer 240

a normal huntington gene has 20 or less CAG repeats but in Huntington’s disease there are 3 types:

1 - 27-35 repeats
2 - 36-39 repeats
3 - over 40 repeats

all the repeats code for a mutant huntington gene with long sticky tail of glutamine which all stick together and form clumps which end up in the nucleus and is thought to disrupt signals and kills cells

the more repeats, the earlier the onset

Question 241

Treatment of Huntington’s disease?

Answer 241

no treatment so aim to relieve symptoms, healthy lifestyle, SSRIs for depression, speech and physical therapy, occupational therapy, benzodiazepienes for chorea, levodopa and dopamine agonists for bradykinesia and rigidity

genetic testing, counselling and education

Question 242

Symptoms of juvenile Huntington’s disease?

Answer 242

parkinsonian features, dystonia, pyramidal tract signs, dementia, epilepsy, mild or absent chorea, behavioural and learning difficulties

Question 243

What is a transient ischemic attack?

Answer 243

a mini/warning stroke, normally last less than 5 minutes and symptoms resolved in 24 hours, caused by brief ischemia from a block blood vessel to the brain, it is not long enough to cause permanent damage

Question 244

Risk factors of TIA?

Answer 244

age, FH, male, alcohol, hypertension, smoking, hyperlipidaemia, DM, obesity, high fat diet, stress, emoboli, south asian, african, caribbean

Question 245

Pathophysiology of TIA?

Answer 245

emboli in carotid artery with existing stneosis and plaques, leads to impaired perfusion of the brain

Question 246

Symptoms of TIA?

Answer 246

contralateral hemiparesis (weakness on opposite side of body), dysarthria (slurred sppech), vision problems, gait disturbance, carotid bruit from atherosclerosis, increased BP, heart murmur

Question 247

Causes of TIA?

Answer 247

atherothromboembolism, caridoembolism, mural thrombus post MI or in AF, valve disease, prosthetic valve, hyperviscosity, polycythamia, sickle cell anemia,, leukostasis, myeloma, vasculitis

Question 248

DD of TIA?

Answer 248

hypoglycaemia, migraine aura, focal epilepsy, hyperventilation

Question 249

Tests for TIA?

Answer 249

carotid US, CT of head, test for hypertension , diabetes, cholesterol, ECG, eye exam, doppler and angiography

Question 250

Treatment of TIA?

Answer 250

prevent stroke - antiplatelets, aspirin, warfarin, clopidogrel, statins for cholesterol, carotid endarterectomy to remove plaque and correct stenosis, intraoperative transcranial Doppler to monitor middle cerebral artery flow, healthy lifestyle, avoid driving for 1 month, antihypertensives, stop smoking and drinking

Question 251

What is amarurosis fugax?

Answer 251

caused by an emboli passing into the retinal artery and causes a temporary loss of vision in one eye due to lack of blood flow to the retina

Question 252

What is the risk of a stroke after TIA based on?

Answer 252

ABCD2 risk
>60(1), BP>140mmHG or 90mmHg diastole(1), unilater weakness(2), speech distubrance without weakness(1), >60mins(2), 15-59mins(1), diabetes(1)

Question 253

What is meningitis?

Answer 253

an inflammation of the lepto meninges and underlying subarachnoid CSF

Question 254

What are the most common pathogens for meningitis for kids, adults, elderly and neonates?

Answer 254

adults - strep. pneumoniae, neisseria meningitis, listeria monocytogenes

kids - listeria monocytogenes, pneumococcus, neisseria meningitis

neonates - group b strep, e.coli

elderly - listeria monocytogenes

mainly viral > bacterial > fungal

aerobic gram negative bacilli associated with trauma/neurosurgery

Question 255

Risk factors for meningitis?

Answer 255

immunocompromised, C5-C9 deficiency, injections, VP shunts, splenectomy, transplants, in crowds, DM, alcoholic, cirrhosis, infection, surgery, itrathecal durgs, tumours, SLE,

Question 256

Symptoms of meningitis?

Answer 256

fever, vomiting, severe headache, stiff neck, dislike of bright lights, seizures, rash, very sleepy/difficult to stay awake, confused/delirious, altered mental sate, non blanching petechial and purpric skin rash, cold hands and feet, papiloedema, Kernigs sign (inability to extend knee when hip is flexed), Brudzinski sign (spontaneous flexion of the hip with active flexion of the neck)

Question 257

DD of stiff neck?

Answer 257

infections in head and neck e.g. pharygitis

Question 258

What are latent viral infections?

Answer 258

VZV, HSV, HIV, priors

Question 259

Toxin mediated diseases?

Answer 259

botulism, tietanus

Question 260

Immune mediated disease?

Answer 260

Guillian Barre, post infection, ADEM, HLE

Question 261

Investigations for meningitis?

Answer 261

CBC w/diff, Chemo10, 2 blood cultures, CT head no contrast (but dont do if no focal neurological findings), LP (but obtain CT first if needed to identify ICP) and CSF studies, gram stain, HSV PCR, cryptococcal Ag, TB PCR, fungal PCR

Question 262

What are bacterial CSF results like?

Answer 262

cloudy/yellow, increasing opening pressure, increased protein, decreased glucose, increased WBC (PMN), gram positive

Question 263

What are viral CSF results like?

Answer 263

cloudy/clear, gram negative, increased lymphocytes

Question 264

What are fungal/TB CSF results like?

Answer 264

cloudy/straw, increased opening pressure, increased protein, gram negative, lymphocyes

Question 265

Complications of meningitis?

Answer 265

hydrocephalus, abscess, cerebritis and cranial nerve lesions, thrombosis, infarct, ventriculitis and ventriculopathy, extra axial collections, seizures, DIC, septic shock, SIADH, decreased hearing

Question 266

DD of meningitis?

Answer 266

malaria, encephalitis, septicaemia, subarachnoid haemorrhage (have blood in csf), dengue, tetanus

Question 267

Management of viral meningitis?

Answer 267

IMMEDIATE ANTIBIOTICS (55 or immunocompromised = cefotaxime and amoxicillin due to listeria risk) - they must be able to pass the blood brain barrier

aciclovir is encephalitis suspected

IV fluids and inotropes if septicaemia

TB meningitis treated for 9 months

dexamethasone if pneumococcal menigitis

vancomycin added if travelled to area of increased pneuomococcal resistance

ganciclovir for CMV infectiosn

corticosteroids if hearing loss and neurological sequelae

benzylpenicillin if penicillin sensitive organiism

Question 268

Which organism has the poorest prognosis in meningitis?

Answer 268

pneuomococcal meningitis

Question 269

What is shingles?

Answer 269

a skin rash caused by infection of the herpes zoster virus (also causes chicken pox)

Question 270

Symptoms of shingles?

Answer 270

pain that precede the rash and rash in a cluster or band, headache, burning/itching in affected skin, fever

Question 271

Cause of shingles?

Answer 271

when the herpes zoster virus becomes reactivated, it normally is dormant, but become reactivated during lowered immunity during stress,

Question 272

How does the shingles rashs progress?

Answer 272

initial red blotches on the skin, just develops into itchy blisters which contain the virus, eventually they become yellow, flatten and dry out, leaving a scab

Question 273

What is ophthalmic shingles?

Answer 273

when it affects one of the eyes when the reactivated virus is in the trigeminal nerve, causing rash over forehead, nose, eye, conjunctivitis, red eye and vision problems

Question 274

How to prevent spread of shingles?

Answer 274

not sharing towels, dont swim or play contact sport, avoid work if rash is weeping and cannot be covered, avoid pregnant women who haven’t had it yet, avoid immunocompromised

Question 275

Treatment of shingles?

Answer 275

antiviral medications e.g.acyclovir, preferably become blisters appear

prednisolone, analgesics, cool wet compresses

zinc containing ointment to dry the blisters

loose fitting clothing

anticonvulsants relieve nerve pain

Question 276

side effects of antivirals?

Answer 276

decreased GFR, vomiting, encepahlopathy, urtcaria, nausea, abdominal pain, dizziness

Question 277

Complications of shingles?

Answer 277

postherpetic neuralgia (severe nerve pain) and intense itching even after rash is gone, pain is in affected dermatomes, can last years and it is intolerable

opthalamic shingles, ramsay hunt syndrome, infection, scarring,

Question 278

At what age are you likely to get shingles?

Answer 278

> 50

Question 279

What is encephalitis?

Answer 279

inflammation of the brain normally due to an infection which can lead to brain damage, swelling, pressure and death

Question 280

Risk factors of encephalitis?

Answer 280

exposure to viruses

Question 281

In who is encephalitis most common?

Answer 281

young or elderly

Question 282

What are the most common viruses to cause encephalitis?

Answer 282

herpes simplex virus, varicella zoster virus, CMV, EBV, HIV, measles, mumps, rabies, japanese B encephalitis, west nile tick, tick borne encephalitis

Question 283

What are non viral causes of encephalitis?

Answer 283

bacterial meningitis, TB, thyphus, malaria, listeeria, Lyme disease, post vaccination, autoimmune ecephalitis, legionella, cryptococcus, vaccination, sphyllis, roundworm

Question 284

Symptoms of encephalitis?

Answer 284

fever, headache, nausea, vomiting, joint pain, seizures, focal neurological deficits, confusion, change in personality, photophobia, hallucinations

Question 285

what are the 3 types of chronic encephalitis?

Answer 285

subacute sclerosing panencephalitis, progressive multifocal leukodystrophy, chronic progressive HIV encephalitis

Question 286

Investigations for encephalitis?

Answer 286

LP - increased CSF protein and lymphocytes, decreased glucose
culture and PCR of HSV within CSF
increased mononuclear cells
EEG - shows diffuse abnormalities
CT contrast - focal bilateral temporal lobe

Question 287

Treatment of encephalitis?

Answer 287

acyclovir within 30 mins for 14days (21days if immunocompromised), supportive therapy, antibiotics, immunoglobulin therapy, plasmapheresis, corticosteroids if autoimmune, sedatives for irritability, physical/speech therapy, immunosuppressants, symptomatic treatment

Question 288

Prognosis of encephalitis?

Answer 288

70% mortality in untreated, 20% mortality in treated

normally lasts for 1-2 weeks, but can take several months to revocer

probable reactivation

Question 289

complications of encephalitis?

Answer 289

permanent brain damage, affecting hearing, memory, msucle control, sensation, speech and vision, personality changes, epilepsy

Question 290

What is rabies and how is it transmitted?

Answer 290

the rhabdovirus RNA virus, transmitted by saliva of animals, which spreads to the CNS via peripheral nerves and forms Negn bodies, it replicates in the grey matter then trans-located to tissues and salivary glands

Question 291

Symptoms of rabies at each stage?

Answer 291

prodomal stage - fever, jeadache, malaise, hyperaethesia at bite site
encephalitis - excitation, hallucinations, lucent period
brain stem dysfunction, cranial never involvement, salivation, hydrophobia

Question 292

Diagnosis of rabies?

Answer 292

biopsy nape of neck or corneal impression smear of fluorescent antibody, salivary viral culture, PCR investigated, non specific serology

Question 293

Treatment of rabies?

Answer 293

exposure prophylaxis, local wound cleaning, vaccine,

Question 294

What is polio and how is it transmitted?

Answer 294

viraemia, types 1, 2 and 3, transmitted by faecal oral route, crosses the blood brain barrier causing meningocephalitis with destruction of motor nuceli of anterior horn of brain stem and spinal cord

Question 295

What complications can polio lead to?

Answer 295

paralytic poliomeylitis, asymeme flaccid paralysis, respiratory muscle involvement

Question 296

Treatment and prevention of polio?

Answer 296

vaccine with life attenuated types 1, 2 and 3, inactivated polio vaccine, 3 doses, boosters

Question 297

What is cerebral toxiplasma, its symptoms and treatment?

Answer 297

reactivation of latent infection, seroprevalence rates 15-50%, CD4 usuallu

Question 298

Treatment of CMV?

Answer 298

ganciclovir

Question 299

What is tetanus?

Answer 299

clostridium tetani, a soil organism infecting via dirty wounds, terminal spore, gram positive anaerobe, ubigulitis, toxin secretor (tetanospasmin) and translocates via the peripheral nerve, binds to GABA receptors of inhibitory interneurone

Question 300

Symptoms of tetanus?

Answer 300

parasthesia of wound, lock jaw, sustained muscle contractins, involvement of facial muscles, paraoxysmal generalised spasm, autoimmune dysfunction

Question 301

Diagnosis of tetanus?

Answer 301

debride wound, benzyle penicillin, human tetanus immunoglobulin, control spasm with dantolen, baclofen, control hypertension, ITU, airway mangement, tetanus toxin vaccination, 3 doses, signle booster

Question 302

What is botulism?

Answer 302

clostridium botulism, spore former, anaerobe, e.g. cans, a neurotoxin seen in IVDU with contaminated heroin, incubation of 18-36 hours

Question 303

Symptoms of botulism?

Answer 303

descending paralysis with cranial neuorpathy first, diplopia, dysrathria, dysphagia peripheral weakeness

Question 304

Treatment of botulism?

Answer 304

equine of human antitoxin

Question 305

Cord compression symptoms?

Answer 305

acute lower back pain precedes then neurological deficits, neuropathic pain, motor and autonomic dysfunction e.g. sensory loss below lesions (one or 2 segments below), tone and reflexes reduced, leg weakness and sensory loss, arm weakness is less severe

Question 306

Investigations for cord compression?

Answer 306

MRI - show site of compression
CXR - shows degenerative bone disease and destruction of vertebrae by infection of neoplasm
biopsy and surgical exploration
serology, ESR, FBC, syphillis serology, serum electrophoresis

Question 307

What is cord compression linked to and why?

Answer 307

cancer patients do to the rich venous plexus which increases haematogenous spread to metastases to the spine

Question 308

Red flag symptoms for cord compression needing urgent referral and why?

Answer 308

bladder dysfunction, sphincter disturbance, saddle anesthesia (numbess to perineal area), bilateral lower extremity weakness

can lead to complete paralysis

Question 309

Treatment of spinal cord compression?

Answer 309

malignancy - dexamethasone IV to reduce oedema around lesion and improve outcome before radiotherpay and chemo with decompressive laminectomy
epidural abscesses surgically decompression
antibiotics
anti inflammatories

Question 310

What is the cauda equina?

Answer 310

it is the nerve roots caudal to the spinal cord temination, provides sensory and motor innervation to the hip muscles, lower extremity muscles, urinary and anal sphincters and muscles for sexual function

Question 311

What is cauda equina syndrome?

Answer 311

compression of the spinal cord or spinal damage from L2 down,

Question 312

What is the most common cause of cauda equina syndrome?

Answer 312

lumbar disc prolapse from lumbar disc herniation at L4/l5 and L5/S1

Question 313

Causes of cauda equina syndrome?

Answer 313

disc herniation, lumbar stenosis, trauma, neoplasm, infection, abscess, inflammatory disease, CIDP, pagets, ankylosing spondylitis, post operative haematoma, spondylolisthesis, sarcoidosis, congenital lumbar disease

Question 314

Symptoms of cauda equina syndrome?

Answer 314

depend on where the lesion is compressing the nerves - weakness, anesthsia/sensory deficiency, pain, paraesthesias, loss of sphincter tone resulting in incontinence, sexual problams, fasciculations, reduced of absent DTRs, saddle numbness, back pain and radicular pain down the legs, sexual dysfunction, reduced cremasteric reflex, reduced sensation over particular dermatomes

Question 315

Investigations for cauda equina syndrome?

Answer 315

MRI to determine level of compression
CXR
CSF analysis if meningismal
Myelography and CT
urodynamic studies to monitor recovery of bladder function post decompression studies

Question 316

DD of cauda equina syndrome?

Answer 316

conus medullaris syndrome, mechanical lower back pain, prolapsed lumbar discm fracture of lumbar verterbraw due to trauma, spinal tumour, spinal cord compression, peripheral neuropathy, guillain barre syndrome, amyoropjhic lateral sclerosis, MS, diabetic neuropathy, spinal neoplasm

Question 317

Risk factors for cauda equina syndrome?

Answer 317

age, cancer patient, trauma,

Question 318

Treatment of cauda equina syndrome?

Answer 318

based on underlying cause, referred to specialist, surgical intervention for trauma, rehabilitation, anti inflammatories, physio, chemo and radiotherapy, lesion debulking for space occupying lesions

Question 319

Complications of cauda equina syndrome?

Answer 319

paralysis, sensory abnormalities, bladder bowel and sexual dysfunction,

Question 320

prognosis of cauda equina syndrome?

Answer 320

based on cause, but poor treatment leads to long term bladder, bowel and sexual dysfunction, and late diagnosis leads to neurological deficit, poorer diagnosis if bilateral sciatica or complete perianal anesthesia than if it was just unilateral pain.

Question 321

What is motor neuron disease?

Answer 321

cluster of degenerative disease with selective loss of neurons in the motor cortex, cranial nerve nuclei and anterior horn cells, upper and low motor neurons are affect but no sesnory loss of sphincter disturbance

Question 322

Difference between MS and MND?

Answer 322

MS has sensory and motor loss and causing sphincter disturbance and MDN only affects motor and no distubrance

Question 323

Difference between mysasnthia gravis and MND?

Answer 323

MND never affects eye movements unlike MG

Question 324

What are the 4 clinical types of MND?

Answer 324

1 - progressive muscular atrophy - LMN lesion, causing weakness, wasting and fasciculation (spontaneous, irregular and brief contractions of part of a muscle) in hands and arms, affects distal first

2 - amyotrophic lateral sclerosis - combination of lateral corticospinal tracts and anterior horn cells producing progressive spastic tetraparesis or paraperesis UMN signs with added LMN signs

3 - progressive bulbar and pseudobulbar palsy - from destruction of UMN and LMN in lower cranial nerves with dysarthria, dysphagia, wasting and fasciculation of the tongue, cranial nerves 9-12

4 - primary lateral sclerosis - rare with progressive tetraparesis, loss of Betz cells in motor cortex so mainly UMN signs with spastic leg weakness and pseudobulbar palsy, no cognitive decline

Question 325

Cause of MND?

Answer 325

5-10% familial, trauma, electric shocks, infection

events at the ALD-FTD locus explain 87% of familial ALS and is autosomal dominant

Question 326

How common is MND?

Answer 326

5/100,000 and rare below 30, increasingly common over 50, often fatal within 2-4years

Question 327

What symptoms are linked to a worse prognosis in ALS MND?

Answer 327

bulbar onset, increased in age, decreased FVC, split hand sign with thumb adrift due to wasting around it

Question 328

What are UMN signs in MND?

Answer 328

spasticity, brisk reflexes, increased plantars

Question 329

What are LMN signs in MND?

Answer 329

signs, wasting, fasciculation on tongue, abdomen, back, thigh

Question 330

Investigations of MND?

Answer 330

diagnosis is clinical, fasciculation is characteritic

EMG shows muscle denervation

MRI excludes structural causes

LP excludes inflammatory causes

Question 331

DD of MND?

Answer 331

cervical spine lesion, idiopathic multifocal motor neuropathy

Question 332

Treatment of MND?

Answer 332

Riluzole - a sodium channel blocker that inhibts glutamate release, slow progression slightly

propantheline and amitriptyline for drooling

ventilatory support helps prolong survival and for resp failure

feeding via PEG helps dysphagia

spasticity drugs

neurlogists, dietitian, physio, speech therapist, palliative care

Question 333

SE of Riluzole?

Answer 333

vomiting, increased pulse, somnolence, headache, vertigo and increased LFTs

Question 334

What is a spinal muscular atrophy?

Answer 334

rare disorder which detroys anterior horn cells of the spinal cord, slowly progressive with symmetrical wasting weakness of the limbs

Question 335

What are the 3 types of peripheral neuropathy?

Answer 335

sensory (affects touch, temperatire, pain and other sensations), motor (affects movement) and autonomic (affects involuntary bodily processes

can have a combination of them at one time e.g. sensorimotor polyneuropathy

Question 336

What is peripheral neuropathy?

Answer 336

group of conditions in which the periopheral nervous system is damaged

Question 337

Symptoms of sensory neuropathy?

Answer 337

tingling in the affected body part, numbeness, reduced feeling of pain and changes in temperature (feet), burning/sharp pain in feet and legs, allodynia (pain from light touch), loss of balance or coordination

Question 338

Symptoms of motor neuropathy?

Answer 338

twitching, muscle cramps, muscle weakness and paralysis, muscle wasting, foot drop

Question 339

Symptoms of autonomic neuropathy?

Answer 339

depends on location, constipation, diarrhea, nausea, bloating, hypotension, tachycardia, excessive or lack of sweating, sexual dysfunction, bowel incontinence, dysphagia

Question 340

What is a mononeuropathy?

Answer 340

affects a single nerve caused by acute compression, particularly where the nerves are exposed anatomically or entrapment where the nerve passes through a relatively tight anatomical passage (carpal tunnel) or caused by direct damage

Question 341

what is the most common form of mononeuropathy?

Answer 341

carpal tunnel syndrome, leading to tingling, pain or numbness in the fingers due to irritation of the median nerve

Question 342

What is mononeuritis multiplex?

Answer 342

a systemic disorder, when 2 or more peripheral nerves are affected and it is a systemic cause

Question 343

Symptoms of carpal tunnel syndrome?

Answer 343

tingling, numbness and pin i the thumb, index finger, middle finger and half of ring finger

discomfort in hand and arm, paraesthesia in hand, dry skin, swelling, hypoaesthesiia, atrophy of muscles, worse pain on repetitive use or in same position, impaired dexterity, drop things a lot, Tinnel’s sign

Question 344

Risk factors for carpal tunnel syndrome?

Answer 344

25% FH, pregnancy, menopause, injuries to wrist, manual labour, playing an intrument, diabetes, arthritis, hypothyroidism, obesity in the young, breast cancer medications, abnormal wrist structure

Question 345

Investigations of carpal tunnel syndrome?

Answer 345

assess ability of hand and arm, look for weakness and wasting around thumb, Tinnel’s sign, flexing wrist or holding above head will cause pain, nerve conduction study, EMG, x-ray, US of median nerve

Question 346

Treatment of carpal tunnel syndrome?

Answer 346

avoid triggers, treat underlying cause, wrist splint to prevent bending of wrist which can aggrevate symptoms, no direct pressure on it, corticosteroids for inflammation (tablets of injection into wrist), carpal tunnel decompression surgery

Question 347

Complications of carpal tunnel syndrome and surgery?

Answer 347

infection, recurring pain, scarring, nerve injury, post op bleeding, failure to separate root of carpel tunnel resulting in persistent symptoms

Question 348

What is a polyneuropathy?

Answer 348

symmetrical disease process, can be sensory, motor or autonomic, and leads to symptoms of numbness, tingling, pins and needles, pain in extremities, unsteadiness of feet, weakness, postural hypotension, urinary retention, erectile dysfunction, diarrhea, dimished sweating, impaired pupillary reponses, cardiac arrhythmias

Question 349

Causes of polyneuropathy?

Answer 349

DM, guillain barre sundrome, toxins, vitamin deficiency, leprosy, renal failure

Question 350

Investigations in polyneuropathy?

Answer 350

FBC, ESR, serum vit b12, glucose, urea, electrolytes, LFTs, nerve conduction tests

Question 351

Cause of vitamin B1 deficiency neuropathy (thiamin)?

Answer 351

chronic alcohol dependent patients when little food is consumed, starvation, beriberi

Question 352

Symptoms of vitamin B1 deficiency neuropathy?

Answer 352

Wernicke Korsakoff syndrome, polyneuropathy and cardiac failure

Question 353

Treatment of vitamin B1 deficiency neuropathy?

Answer 353

thiamin for 3 days, anaphylaxis in parenteral thiamin, given before IV glucose in high risk patients

Question 354

Causes and treatment of vitamin E6 deficiency neuropathy (pyridoxine)?

Answer 354

isoniazid therapy for TB, give prophylactic pyridoxine with isoniazid, it mainly cuases a sensory neuropathy

Question 355

Symptoms of vitamin B12 deficiency neuropathy?

Answer 355

polyneuropathy with subacute combined degeneration of the cord, distal sensory loss, absent ankle jerks, evidence of cord disease

Question 356

Treatment of vitamin B12 deficiency neuropathy?

Answer 356

IM vit B12 to reverse peripheral nerve damage but has little affect on the CNS

Question 357

What is hereditary sensorimotor neuropathy?

Answer 357

large and complex group with variable mutations, most common being Charcit-Marie-Tooth disease (peroneal muscular atrophy)

Question 358

Symptoms of hereditary sensorimotor neuropathy?

Answer 358

distal limb wasting and weakness that progresses over many years, mostly in legs with variable loss of sensation and reflexes, legs can resemble inverted champagne bottles due to the wasting

Question 359

What are the 2 types of diabetic neuropathy?

Answer 359

progressive and reversible

Question 360

What are the 2 types of progressive diabetic neuropathy?

Answer 360

symmetrical sensory polyneuropathy and autonomic neuropathy

Question 361

What are the 3 types of reversible diabetic neuropathy?

Answer 361

acute painful neruopathy, mononeuropathy and mononeuritis multiplex with cranial nerve or isolated peripheral never lesions, diabetic amyotrophy

Question 362

What causes isolated mononeuropathies?

Answer 362

occlusion of the vase nervorum (small arteries that supply the peripheral nerves)

Question 363

Where do diffuse neuropathies occur from?

Answer 363

accumulation of fructose and sorbitol (metabolized from glucose in the peripheral nerve) which disrupts the structure and function of the nerve

Question 364

What is the most common form of neuropathy?

Answer 364

symmetrical mainly sensory neuropathy

Question 365

Symptoms of symmetrical mainly sensory neuropathy?

Answer 365

affects the feet first, loss of vibration sense, pain sensation and temperature sensation in the feet, then ‘walking on cotton wool’ and lose balance due to impaired proprioception, hand involvement is uncommon.

Question 366

Complications of symmetrical mainly sensory neuropathy?

Answer 366

trauma, blistering from ill fitting shoes causing ulceration, abnormal mechanical stress, repeated minor trauma, neuropathic arthropathy (Charcot’s joints) in ankle and knee, distorted foot with high arch, clawing of toes, insensitive foot ulceration

Question 367

What is acute painful neuropathy’s symptoms and treatment?

Answer 367

burning or crawling pains in lower limbs, worse at night and with bed clothes pressure, treat with good diabetic control, tricyclic antidepressants, gabapentin and carbamazepine

Question 368

Which are the most common cranial mononeuropathies and their presentation?

Answer 368

3rd and 6th, which supply the extraoccular muscles, presenting with unilateral pain, ptosis and diplopia with sparing of pupillary function

Question 369

Symptoms of diabetic amyotrophy?

Answer 369

painful wasting, usually asymmetrical, or quadriceps, wasting may be marked and knee reflexes may be diminished or absent

Question 370

Symptoms of autonomic neuropathy?

Answer 370

affects CV system (tachycardia, loss of sinus arrhythmia, postural hypotension, peripheral vasodilation), GI (diarrhea, gastroparesis and intractable vomiting), bladder (incomplete emptying) and male ED - treatment is symptomatic

Question 371

Treatment of peripheral neuropathy?

Answer 371

treat symptoms, physio, splints, viagra, male prosthesis, catheter, botulinum toxin, stand up slowly, amitiptyline, duloxteine, pregabalin, tramadol, lidocaine plasters

Question 372

What is a stroke?

Answer 372

a rapid onset of neurological deficit caused by blood flow to the brain being stopped by a blockage or rupture

Question 373

What are the types of stroke and what causes them?

Answer 373

ischemia - caused by blockage from emboli of thrombus

haemorrhagic - caused by breakage in blood vessel in the brain of the membrane surrounding the brain

intracranial venous thrombus - caused by space occupying lesion in the brain e.g. tumoru, abscess, MS

carotid or vertebral artery dissection - allowing blood to track the wall of the artery and occlude the lumen - 20% of young strokes

Question 374

What is the difference between a completed stroke and evolutary stroke?

Answer 374

a completed stroke has reached it’s maximum in 6 hours, turns into evolution when the signs and symptoms are getting worse, usually within 24 hours of onset

Question 375

What is classed as a mini stroke?

Answer 375

patient recovers without a significant neurological deficit and recovers in about 1 week

Question 376

Symptoms of a stroke?

Answer 376

difficulty walking, loss of balance and coordination, dysarthria and difficulty understanding, unilateral face paralysis and weakness, blurred or darkened vision, sudden headache with nausea, vomiting and dizziness

Question 377

Common symptoms for a cerebral stroke?

Answer 377

sensory loss, hemiplegia, dysphagia, homonymous hemianopia, visual spatial deficit

Question 378

Common symptoms in a brainstem stroke?

Answer 378

quadriplegia, disturbances of gaze and vision, locked in syndrome

Question 379

Common symptoms in Lacunar stroke?

Answer 379

ataxic hemiparesis, pure motor, pur sensory, sensorimotor and dysarthria

Question 380

Risk factors for stroke?

Answer 380

hypertension, DM, smoking, hyperlipidaemia, obesity, oestrogen containing oral contraceptive, excessive alcohol consumption, polycythaemia, atrial fibrillation, migraine, vasculitis, cocaine, antiphospholipid syndrome, thrombophilia

Question 381

Investigations in a stroke?

Answer 381

check reflexes, vision, speaking and senses, check for carotid bruit which indicated abnormal blood flow, blood tests, angiogram to find location of black, carotid US, CT, MRI, ECHO, carotid artery stenosis, doppler uS (>70% stenosis is significant), vasculitis shows increased ESR and ANA positive, hyperviscosity with polycythaemia and sickle cell disease

Question 382

Complications of a stroke?

Answer 382

difficulty speaking, moving, thinking which can improve but others need care, aspiration pneumonia, contractures, depression, constipation, stress in spouse

Question 383

Immediate treatment of stroke?

Answer 383

protect airway, urgent CT/MRI, thrombolysis, nil by mouth, hydrate, antiplatelets

Question 384

Primary prevention of stroke?

Answer 384

control risk factors, antihypertensives, treat DM and hyperlipidaemia, exercise, folate supplements, smoking cessation, lifelong anticoagulation if rhuematic or prosthetic heart valves, chronic non rheumatic atrial fibrillation

Question 385

Secondary prevention of stroke?

Answer 385

antiplatelet drugs e.g. clopidogrel monotherapy, anticoagulation, lower BP, repair ruptured blood vessel, remove blockage with clot dissolving drugs or blood thinners

Question 386

What is the mortality after 1st stroke?

Answer 386

12% die by day 56

Question 387

What are primary causes of headache?

Answer 387

migraine, cluster or tension type

hemicrania continua, new daily persistant headache, chronic paraoxysmal hemicrania

Question 388

Secondary causes of a headache?

Answer 388

meningitis, subarachnoid haemorrhage, GCA, idiopathic intracranial hypertension, medication overuse, low CSF pressure, post traumatic

Question 389

Red flags in headache history?

Answer 389

> 50, HIV, cancer, trauma, change in personality, vomiting, jaw claudication, severe eye pain, change in frequency, postural, sudden onset, exercise, focal neuorlogical symptoms, fever, altered consciousness, neck stiffness etc

Question 390

What does a thunderclap headache suggest?

Answer 390

subarachnoid haemorrhage

Question 391

Symptoms of idiopathic intracranial hypertension?

Answer 391

not benign, headache with raised ICP, visual disturbance with acuity/fields, papilloedema, normal constituents of CSF

Question 392

Risk factors of idiopathic intracranial hypertension?

Answer 392

obesity, drugs e.g. tetracycline

Question 393

idiopathic intracranial hypertension management?

Answer 393

modify risk factors, monitor visual fields with Goldman fields, acetazolamide/topiramate/diuretics

repeated LPs, CSF shunt, optic nerve fenestration

Question 394

GCA criteria?

Answer 394

> 50, new headache with localised pain, tenderness, decreased pulsation, raised ESR, abnormal biopsy

Question 395

What is a chronic daily headache?

Answer 395

headache on 15 or more day per month

Question 396

How common are migraines?

Answer 396

1/4 women and 1/12 men develop it at some point, commonly starts in childhood or as a young adult, many stop in adult life, can be several attacks a week or once every few years

Question 397

What are the 2 types of migraine?

Answer 397

with aura (classic) and without aura (common)

Question 398

Symptoms of a migraine (without aura)?

Answer 398

headache on one side of head, typically at front or side, sometimes both, then spreads all over, throbbing pain

nausea, vomiting, photophobia, being off food, blurred vision, poor concetration, stuffy nose, hunger, abdo pain, pale, sweating

Question 399

When is migraine pain worse?

Answer 399

most often in morning, but can be at any time, then gradually gets worse and peaks 2-12 hours after and then eases off, can last from 4-72 hours

Question 400

What is a migraine with an aura?

Answer 400

a warning sign before a migraine, which can be visual, numbness, speech, smells etc lasts a few minutes but can last up to an hour, then the migraine develops soon after

Question 401

Examples of migraine auras and which are most common?

Answer 401

visual aura - temporary loss of vision, flashed of light, objects rotate, shake or boil

numbness, pins and needles, travel up the arm and involve face, lips and tongue

problems with speech

old smells, food craving, feeling odd

Question 402

What are the phases of a migraine?

Answer 402

irritability, aura, headache, irritable

Question 403

What are less common types of migraine?

Answer 403

menstrual - only during periods
abdominal - in children, with nausea, and turns to normal migraine in later years
ocular - temporary loss
hemiplegic - severe, on one side of the body, can cause severe dizziness, double vision, hearing problems
basilar type - in the back of the head

Question 404

What causes an aura?

Answer 404

narrowed blood vessels in the brain, which then soon dilate, causing the headache

Question 405

Causes/triggers of migraine?

Answer 405

increased signals in the brain, confusing the brain, familial, dieting too fast, irregular meals, smokey rooms, glaring light, flickering TV, loud noises, depression, tiredness, stress, HRT, contraceptibe pill, periods, shift work, bad sleep patterns, menopause

Question 406

Treatment of migraine?

Answer 406

paracetamol, aspirin, NSAISs, anti emetics, oral triptam medicine e.g. almotriptan which interfere with 5HT (don’t take too early on in attack though),

CI in pregnant women, even though migraine can rarely be worse in pregnancy but migraine improves in most cases with pregnacy and breatfeeding

Question 407

Preventative treatment for a migraine?

Answer 407

topiramate or propanolol, acupuncture, amityriptaline, riboflavin, botulinum toxin type A

Question 408

How common is a tension type headache?

Answer 408

the most common type of headache, 50% of adults have it at least every month and 1/30 adults have chronic tension type headaches

Question 409

What is the difference between episodic and chronic type headache?

Answer 409

episodic = occur on less than half of the days in the month

chronic = occur more than half of the days in the month

Question 410

Symptoms of tension type headache?

Answer 410

band across the forehead, uncomfortable, tiring, worse on activity, sensitive to light and noise, sore neck

Question 411

How long do tension type headaches last for?

Answer 411

from few hours to several days, usually a few hours, they don’t disturb sleep and most people can work through them, you are normally well in between headache

Question 412

Cause of tension type headache?

Answer 412

tightness of neck muscles or ones over the scalp, poor posture, stress, anything that can make the back of the neck muscles tense, may be more genetically prone to develop them due to being stressed and anxious, painkillers too often due to increasing the number of pain receptors in the head and they become excessively sensitive

Question 413

When should a tension headache suggest something more serious?

Answer 413

significant head injury in past few months, pain getting worse, accompnaying fever, problems with speech, balance or memory, headache start when coughing/sneezing, worse when sitting or standing, red or painful eyes, worse headache than ever, low immunity, previous cancer

Question 414

Lifestyle treatment of tension headache?

Answer 414

exercise, change routine, shoulder massage, hot flannel on neck, warm batch, less caffeine, balanced diet, more water, less pillows, avoid excessive noise and reading in low light, diary of frequent headaches, avoid stress triggers

Question 415

Treatment of tension headache?

Answer 415

paracetamol but not for more than a couple of days at a time, codeine, amitriptyline

Question 416

What is a cluster headache?

Answer 416

severe unilateral pain, localised in or around the eye with ipsilateral autonomic features, rare

Question 417

What is an episodic cluster headache?

Answer 417

occurs in periods lasting from several days to one year, usually 2-9 weeks, separated by pain free periods of a month or longer

Question 418

What is a chronic cluster headache?

Answer 418

CHs occuring for one year without remission or short lived remissions of less than a month (can start as this or develop from episodic)

Question 419

How common is cluster headache?

Answer 419

rare, 1/1000, more men than female, with a bigger difference between them in chronic then episodic but episodic being more common overall, usually occurs 20-40 years

Question 420

What signs suggest an episodic cluster headache is turning into chronic?

Answer 420

later onset, sporadic attacks occur, higher frequency of cluster periods, shorter periods of remission

Question 421

Causes of cluster headache?

Answer 421

1/20 have a 1c family member, associated with HCRTR2 gene

Question 422

Pathophysiology or cluster headaches?

Answer 422

ipsilateral hypothalamic grey matter has dysfunction causing dilation of cranial vessels mediated by trigeminoparasympathtic reflexes, changes in melatonin in relation to the light and dark cycle affect CH

Question 423

Clinical features of cluster headaches?

Answer 423

rapid onset of pain over 10 minutes which maintains intensity, excruciating, sharp and penetrating, centered behind the eye/temple/forehead (occasional neck), unilateral pain, lacks 45-90 minutes, 1-2x/day

ipsilateral lacrimation, rhinorrhoea, nasal congestion, eyelid swelling, facial sweating, flushing, conjunctival injection

restless (unlike migraine), band head against wall, nausea

Question 424

Triggers of cluster headaches?

Answer 424

alcohol, heat, exercise, solvents, disruption of sleep habits

Question 425

What is the diagnostic criteria of a cluster headache?

Answer 425

for at least 5 attacks:
severe unilateral orbital, supaorbital and/or temporal pain lasting 15-180 minutes if untreated
and at least one:
Ipsilateral conjunctival injection and/or lacrimation.
Ipsilateral nasal congestion and/or rhinorrhoea.
Ipsilateral eyelid oedema.Ipsilateral forehead and facial sweating.
Ipsilateral miosis and/or ptosis
Restlessness or agitation.
One every other day to eight times daily.

Question 426

DD of CH?

Answer 426

paroxysmal hemicrania

short lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)

Question 427

Red flags of a headache?

Answer 427

change in pattern of headache, new headache aged 50, seizures, headache with systemic illness, personality change, raised ICP symptoms, worst headache ever

Question 428

Management aim of CH?

Answer 428

suppress attack and reduce frequency and severity of attack

Question 429

Management of CH?

Answer 429

stop smoking, abstain from alcohol, regular sleep pattern and good hygiene

acute attack - SC sumatriptam and 100% o2, antiinflammatories, lidocaine

Question 430

Prophylaxis of CH?

Answer 430

verapamil, ECG monitoring, prednisolone, lithium is verapamil not effective, melatonin, sodium valproate in chronic, ergotamine before predicted attack, deep brain stimulation, trigeminal nerve blockage, acupuncture

Question 431

Side effects of verapamil?

Answer 431

constipation, flushing

Question 432

What is a subarachnoid hemorrhage?

Answer 432

a spontaneous arterial bleed into the subarachnoid space

Question 433

How common and in who does subarachnoid hemorrhage occur?

Answer 433

6/100,00 pa, usually around 50years and more common in women

Question 434

Causes of subarachnoid hemorrhage?

Answer 434

rupture of berry aneurysm (80%) or congenital arteriovenous malformations

Question 435

Symptoms of unruptured aneurysm?

Answer 435

sight problems, pain on one side of face or around the eye, persistent and severe headaches, painful third nerve palsy, nausea, vomiting, loss of consciousness, meningeal irritation, focal neurological signs, sub hyaloid haemorrhages between the retina and vitreous membrane with or without papilledema, coma, drowsiness

Question 436

Risk factors for subarachnoid hemorrhage?

Answer 436

smoking, high blood pressure, excessive alcohol consumption, family history, bleeding disorders, mycotic aneurysm, post menopause from decrease in oestrogem, ADPKD, Ehlers Danlos Syndrome, coartation of aorta

Question 437

Investigations in subarachnoid hemorrhage?

Answer 437

CT shows subarachnoid blood, lumbar punctureshows biliruibin or oxyHb, must be at least 12 hours after symptoms so that Hb can degrade into the bilirubin and turn the CSF xanthochromic (yellow) which can then be detected by spectrophotometry of the supernatant after centrifugation, should therefore be protected from light, MRA find the source of the bleeding

Question 438

Treatment of subarachnoid hemorrhage?

Answer 438

hydrate to maintain cerebral perfusion, treat hypertension, CCB (nimodipine), analegics, anticonvulsants, antiemtics, intracranial stents, neurosurgical clipping, endovascular coiling, occupational therapist, antidepressants, CBT

Question 439

What is the difference between neurosurgical clipping and endovascular coiling?

Answer 439

clipping to shut off the aneurysm to prevent it growing or rupturing again
coiling inserts a catheter into an artery in the leg into head and passes coils through the aneurysm so blood can’t enter it again so cant rupture, it has increased survival over clipping but increased risk of bleeding

Question 440

Complications of subarachnoid hemorrhage?

Answer 440

rebleeding (commonest cause of death), delay cerebral ischemia from vasospasm causing vessel to narrow, hydrocephalus, hyponatraemia, epilepsy, cognitive dysfunction, depression, PTSD

Question 441

Prognosis of subarachnoid hemorrhage?

Answer 441

50% die suddenly or soon after haemorrhage, 10-20% from rebleeding, variable outcome, glasgow coma score on admission has the most prognostic significance which checks level of consciousness and brain injury severity (12 or more has good prognosis)

Question 442

What 3 things does the Glasgow coma scale base on?

Answer 442

eye opening response, best verbal response, best motor response

Question 443

What is a subdural haematoma?

Answer 443

where the blood collects in the subdural space following a rupture of a vein running from the hemisphere to the saggital sinus, increasing pressure on the brain (intracranial hypertension) causing brain damage (head injury)

Question 444

When do symptoms occur in subdural haematoma?

Answer 444

develop soon or can be days or weeks after

Question 445

Symptoms of subdural haematoma?

Answer 445

progressively bad hangover, feeling and being sick, confusion, personality changes, drowsiness, speech problems, problems with vision, paralysis on one side of the body, problems with walking, frequent falls, seizures, loss of consciousness, localising neurlogical symptoms (unequal pupils)

Question 446

In who is subdural haematoma most commonly seen?

Answer 446

older, blood thinning medication, drink excessively, accident prone, atrophic brains which makes the connecting veins more susceptible to rupture due to the increased tension

Question 447

Diagnosis of subdural haematoma?

Answer 447

CT and MRI to rule out other illnesses

shows clot and midline shift and a CRESCENT shape collection of blood over 1 hemisphere

Question 448

Treatment of subdural haematoma?

Answer 448

surgery to remove haematoma, or if small, monitor to see if they can heal spontaneously

Question 449

Complications of subdural haematoma surgery?

Answer 449

further bleeding on the brain, infection, deep vein thrombosis, seizures, stroke

Question 450

What is an extradural hemorrhage?

Answer 450

an injury that fractures the temporal bone and ruptures the underlying middle meningeal artery causing a collection of blood in the potential space between dura and bone

Question 451

In who is extradural hemorrhage seen?

Answer 451

males, rare in small children due to the plasticity of the skull, less common over 60 due to dura being tightly adherent

Question 452

What happens shortly after an extradural hemorrhage?

Answer 452

there is a brief period of unconsciousness followed by a lucid interval of recovery which can be a few hours to a few days before a bleed with decrease GCS from rising ICP with rapid deterioration with focal neurological signs and deterioration in consciousness level if surgical drainage is not immediately carried out

Question 453

What causes a spontaneous extradural hemorrhage?

Answer 453

a coagulation or platelet defect

Question 454

Symptoms of extradural hemorrhage?

Answer 454

increasingly severe headache, nausea, vomiting, seizures, confusion, bradycardia indicating raised ICP, skull fractures, haematomas, lacerations, CSF otorrhoea or rhinorrhoea, alteration in consciousness and deterioation of the glasgow coma scle, unequal pupils, facial never injury, weakness of limbs, hemiparesis, visual field defects, numbness, coma, death from respiratory arrest

Question 455

Investigations of extradural hemorrhage?

Answer 455

x ray - skull fracture, fracture lines crossing the middle meningeal vesicles
ct san - haematoma LENS SHAPE (not sickle like subdural) as the tough dural attatchments to the skull keep it more localised
MRI -
AVOID LUMBAR PUNCTURE
fbc, u and e

Question 456

Management of extradural hemorrhage?

Answer 456

ABC, O2, full trauma assessment, IV fluids to preserve cerebral perfusion, osmotic diuretics if ICP raised, intubation and ventilation and mannitol if ICP decreased, Burr holes to evacuate haematoma, DVT prophylaxis

Question 457

Complications of extradural hemorrhage?

Answer 457

neurological deficits (temporary or permanent), death, PTS seizures 1-3 months post injury

Question 458

What are delayed effects of extradural hemorrhage?

Answer 458

post concussion syndrome which has headaches, dizziness, vertigo, restlessness, emotional liability, inability to concentrate and fatigue

Question 459

Symptoms of spinal extradural hemorrhage?

Answer 459

spasticity, neuropathic pain, urinary complications

Question 460

Prognosis of extradural hemorrhage?

Answer 460

excellent in children, low GCS is bad prognosis, prognosis worse if older, intradural lesions, volume of haematoma, temporal location, rapid clincal porogrssion, pupillary abnormalities, increased ICP

Question 461

What are Charcot Bouchard aneurysm?

Answer 461

0.3-0.9mm, a hypertensive hemorrhage arising from deep perforator arteries that can lead to lacunar infarct, microbleeds and hemorrhage

Question 462

What are lobar haemorrhages?

Answer 462

large and superficial, common in elderly people

Question 463

Treatment of an anticoagulant related ICH?

Answer 463

warfarin check urgent INR, consider reversal with Beriplex and vitamin K, if low platelets have platelet transfusion

Question 464

Treatment of infratentorial bleed with brainstem compression?

Answer 464

surgical decompression

Question 465

Treatment of hydrocephalus?

Answer 465

external ventricular drain

Question 466

When should a neurosurgeon be called in a hemorrhage?

Answer 466

deteriorating GCS, hydrocephalus, coning, large cerebellar hemorrhage >3cm, distortion of the 4th ventricle with gcs >8

Question 467

How are head injuries classified?

Answer 467

on type of injury, distribution of the lesions, time course of damage following the traumatic event

Question 468

What are the types of distribution of head injuries?

Answer 468

focal:
scalp - contusions, lacerations
skull - facture
meninges - haemorrhage, infection
brain  - contusion, lacerations, hemorrhage, infection 

diffuse: 
diffuse axonal injury
diffuse vascular injury
hypoxia-ischemia
swelling

Question 469

What does a focal head injury suggest?

Answer 469

considerable force, increased risk of haematoma and infection and aerocele

angled or pointed objects cause localised fractures that are open or depressed

flat surfaces cause linear fractures that can extend into skull base and be called contrecoup factures

Question 470

What is the difference in focal brain damage mechanisms?

Answer 470

contact damage - at or just deep to point of impact

acceleration/deceleration damage - causes differential movement of skull, brain and brain tissue causing traction and damage blood vessels

contusions - superficial bruises of the brain, coup at site of impact/contre coup away from site of impact, first become haemorrhagic then become brown and soft then indented and cavitated after months

lacerations - when the contusion is sufficientlu severe to tear the pia mater

Question 471

What are the different types of diffuse lesions?

Answer 471

diffuse axonal injury - a clinicopathological syndrome of widespread axonal damage

diffuse traumatic axonal injury

traumatic axonal inury - involving acceleration and decelaration

axonal injury

swelling - increasing ICP, caused by vasodilation, increased cerebral blood volume, extravasation of oedema fluid from damaged vessels, increased water content of neurons and glia

hypoxia-ichemia -

diffuse vasuclar injury - results in near immediate death, multiple petechial hemorrhages throughout the brain

Question 472

What causes herniation?

Answer 472

bleeding and brain swelling

Question 473

What is a missile head injury?

Answer 473

can be a depressed injury that does not penetrate the skull, penetrating injuries, or perforating injuries

Question 474

What is chronic traumatic ecephalopathy?

Answer 474

a neurodegenerative condition seen 8-10 years after repetitive mild traumatic brain injury, 1/3 are progressive

initally irritability, impulsivity, aggression, depression, memory loss

e.g. dementia, gait, speech problems, parkinsonism

Question 475

How does chronic traumatic encephalopathy appear?

Answer 475

an atrophic neocortex, hippocampus, diencephalon and mamillary bodies

enlarged ventricles with fenustrated cavuum septum

tau positive neurofibrillary and astrocytic tangles

frontal and temporal cortex and limbic regions especially around depths of sulci and limbic regions

Question 476

What is dystonia?

Answer 476

a state of abnormal muscle tone resulting in muscular spasm and abnormal posture usually caused by a neurological disease, side effect of drug therapy and trauma

Question 477

Why does vibration induce illusion of movement?

Answer 477

either subnormal muscle spindles responsiveness to stretch improves with fatigue of the muscle or subnormal responsiveness of the CNS to the afferent input improves after fatigue of muscle

Question 478

What is dopa dysregulation syndrome?

Answer 478

result of presynaptic neuron loss and post synpatic receptor supersensitivity

Question 479

Symptoms of anterior carotid artery stroke?

Answer 479

leg weakness, sensory disturbance in legs, gait apraxia, truncal ataxia, incontinence, drowsiness, akinetic mutism, decrease in spontaneous speech, stuporus state

Question 480

Symptoms of middle carotid artery stroke?

Answer 480

contralateral arm and leg weakness, contralateral sensory loss, hemianopia, aphasia, dysphasia, facial droop

Question 481

Symptoms posterior carotid artery stroke?

Answer 481

contralateral homonymous hemianopia, cortical blindness with bilater involvement of the occipital lobe branches, visual agnosia, prosopagnosia, dyslexia, anomic, aphasia, colour naming, discrimination problems, unilateral heaches

Question 482

Symptoms of posterior circulation strokes?

Answer 482

motor deficits, dysarthria, speech impairment, vertigo, nausea, vomiting, visual disturbances, altered consciousness

Question 483

What makes up a muscle?

Answer 483

muscle fibres, which are long multinucleated structures bound by sarcolemma

Question 484

What are myofibrils?

Answer 484

the contractile element within the myofibre, with thin (I actin) or thick (A myosin) filaments, they are multinucleated and bound by sarcolemma

Question 485

How do myofibrils work?

Answer 485

excitation force along the whole length simultaneously, and release calcium from SR, it is a T tubule system with invaginations of sarcolemma

Question 486

What mechanisms can cuase muscular dystrophies?

Answer 486

loss of structural proteins, defective enzymes, disruption of sarcolemma repair, loss of signalling molecules, non coding region mutations, defective post translational modifications

Question 487

What is a muscular dystrophy?

Answer 487

a group of familial disorders causing replacement of muscle tissue with fibrous connective tissue causing progressive muscle weakness and muscle wasting

Question 488

What is Duchenne muscular dystrophy?

Answer 488

X linked inheritance (Xp21), muscle degeneration, large deletions and duplications and point mutations disrupting the reading frame causing absence of dystrophin (which connects cytoskeleton to ECM to protect the muscle during force of contraction)

Question 489

What is the most common muscular dystrophy in children and the prognosis?

Answer 489

DMD 1/3500 males, manifesting at 5 years of age, leading to wheelchair dependence by 13, survival is rare over 30

Question 490

Symptoms of DMD?

Answer 490

muscle degeneration, thin weak thighs, tip toeing, weak stomach muscles causing stomach to protrude out, shoulders and arms back awkwardly, swayed back, weak butt muscle pushing body out further, thick calves from fat, tight leg muscles, poor balance, awkward walking, cardiac involvement

Question 491

What is Beckers muscular dystrophy?

Answer 491

DMD but less severe, slower progression, later onset in 20s, and death around 40, worse cardiac involvement

Question 492

What is myotonic dystrophy?

Answer 492

autosomal dominant, with a CTG trinucelotide repeat expansion in DMPK on c19, most common muscular dystrophy in adults

mutation causes RNA toxicity, downstream, effect causing missplicing of proteins, the CLCN1 is misspliced

Question 493

Symptoms of myotonic dystrophy?

Answer 493

sustained involuntary contraction (difficult releasing grip after hand shake) as the muscles are still contracting, prominent forehead, narrow face, boldness, cataracts, poorly developed chin, dysphagia and difficulty breathing, diabetes, frontal balding

Question 494

Treatment of DMD?

Answer 494

supportive, scoliosis corrective surgery in children, manage heart problems, NIV for resp failure, steroids (prednisolone with slows down disease progression given when motor functions plateau), gene therapy (anti sense oligonucleotides weekly sc injections to promote ribosomal read)

Question 495

Treatment of MD?

Answer 495

supportive, treat cardiac complications, experimental AON knows down expansions, fleicanide of mexilitine for symptom relief of myotonia

Question 496

What is facialscapulohumeral muscular dystrophy?

Answer 496

autosomal dominant, presenting at 20 years, 20% need a wheel chair, normal life expectancy, contraction in macrosatallite repeat D4Z4 on 4q35, only occurs if polyadenylated, usually 11-100 repeats but only

Question 497

Symptoms of FSHD?

Answer 497

scapular fixators and ankle dorsiflexor weakness, retinal telangectasia and sensorineural hearing loss

Question 498

What is acute pain?

Answer 498

sudden onset, in response to injury and infection which resolves as the condition resolves, recurrent acute pain is not chronic pain

Question 499

What is chronic neuropathic pain?

Answer 499

a neurological condition resulting from damage to or dysfunction of the sensory nervous system, persists in the absence of tissue damage

Question 500

Clinical features of chronic neuropathic pain?

Answer 500

burning hot and cold sensations, electric shocks, shooting pains, deep severe ache, poorly localised, numbness, paraesthesiae, recognisable dermatomal pattern, skin area may be hypersensitive, exacerbated by contact with hot or cold air, worse at night, distracted by activity associated with depression

Question 501

What increases risk of chronic pain?

Answer 501

cultural beliefs, ongoing litigation, claims, benefits, work pressures, social circumstances, family support

Question 502

What causes chronic neuropathic pain?

Answer 502

poorly understood level of damage to sensory pathway, pain fibres small unmyelinated C fibres, increased afferent activity or increased synaptic transmission at level of spinal cord in pain pathway

Question 503

Neuropathic pain terms?

Answer 503

neuralgia, neuropathy, hyperalgesia, causalgia, hyperpathia, allodynia, lumbagp

Question 504

Chronic pain management?

Answer 504

try and find cause, neurological examination to identify nerve root compression, X rays, MRI spine, serology, MDT approach, pain management programme, reassurance, encourage activities, exercise

drugs - opioids (pre synaptic inhibition), antidepressants, anti convulsants, N-Methyl D-aspartate receptor antagonists (pre synaptic excitation)

nerve blocks to support physiotherapy and increased activities, TEN stimulators, spinal cord nerve stimulator implantation, dorsal column fiber ablation

capsaicin topical cream and lignocaine gel, acupuncture

Question 505

Prevention of chronic pain?

Answer 505

regional blocks as an adjuvant to surgery to reduce post amputation phantom limb pain, peri operative gabapentin or pregabelin, holistic approach to surgery

Question 506

Tolerance to opioid analgesic drugs?

Answer 506

tolerance, increased metabolism, down regulation of opioid receptors, neuroplasticity of CNS target areas

Question 507

What is involved in the aortic arch?

Answer 507

the brachiocephalic trunk dividing into the right common carotid and subclavian arteries and the aortic arch splits into the left common carotid, subclavian and vertebral

Question 508

At what level do the common carotid arteries bifuricate?

Answer 508

C3-C4

Question 509

What are the different point of the internal carotid and their characteristics?

Answer 509

cervical - no narrowings, dilations or branches, lies posterior and lateral to ECA at origin, ascending behind then medial to the ECA

petrous - penetrates temporal bone, running horizontally in the carotid canal, small branch to middle/inner ear, vidian artery to ECA

cavernous - turns superiorly at foramen lacerum entering cavernous sinus, piercing dura, small branches supply dura, cranial nerves 3-6 and posterir pituitary, and connects to ECA via ILT

supraclinoid - opthalmic artery (to optic canal), superior hypophyseal (to pituitary gland, stalk, hypothalamus, optic chiasm), posterior communicating artery and anterior chorodial artery (choroid plexus, optic tract, cerebral peduncle, internal capsule, medial temporal artery)

Question 510

What does the middle cerebral artery supply?

Answer 510

the lateral lenticulostriate arteries (lentiform nucleus, caudate nucleus, internal capsule), insular cistern, onto brain surface to supply vessel on brain surface

Question 511

What does the anterior middle cerebral artery supply?

Answer 511

medial lenticulostriate arteries to supply head of caudate nucleus and internal capsule, recurrent artery of Heubner, cortical branches from calllosomarginal and pericallosal arteries

Question 512

What do the extra cranial VA branches supply?

Answer 512

neck muscles, spinal meninges, spinal cord, anastomoses with other neck vessels

Question 513

Where do verterbral arteries arise from?

Answer 513

the subclavian arteries (left can arise directly from arch)

Question 514

What are the intracranial VA branches?

Answer 514

anterior spinal artery, small meduallry perforators and posterior inferior cerebellar artery to supply the medulla and the inferior cerebellum

Question 515

What does the posterior cerebel artery supply?

Answer 515

cortical territories including the inferior temporal lobe, posterior third of the interhemispheric surface and visual cortex and occipital lobe

Question 516

How many vertebrae and nerves are in each of the spinal cord?

Answer 516

cervial - 7 - 8
thoracic - 12 - 12
lumbar - 5 - 5
sacral - sacrum - 5
coccygeal - coccyx - 1

Question 517

What structures are in the grey and white mater?

Answer 517

grey - dorsal horn, intermeddiate zone, ventral horn, lateral horn

white - dorsal funiculus, dorsolateral funiculus, ventrolateral funiculus, ventrolmedial funiculus

Question 518

How do the internal structure differ in the spinal cord?

Answer 518

white mater decreases down the spine, grey mater increased in the cervical and lumbosacral enlargements, lateral horn is present in the thoracic and upper lumbar segments

Question 519

What is a stretch reflex?

Answer 519

monosynaptic reflex, important postural reflex, basis of tendon jerk

Question 520

What is a flexor reflex?

Answer 520

polysynaptic reflex, withdrawal of a limb in response to pain

Question 521

What is the ventral horn?

Answer 521

receives >20,000 synaptic contacts, has primary efferent tracts from the dorsal root, with interneurons and descending tracts, primary sensory afferent neurones

Question 522

What are the fasciculus cuneatus and gracilis do?

Answer 522

ascending fibres, ipsilateral

discriminative touch, sensation and proprioception

cuneatus (lateral) - arms
gracilis (medial) - legs

Question 523

Name nerves?

Answer 523

olfactory -s
optic - s
occulomotor - m
trochlear - m
trigeminal nerve - opthalamic, mandibular, maxially - b
abducens - m
facial - b
vestibulacochlear - s
glossopharengeal - b
vagus - b
accessory - m
hypoglossal - m

Question 524

Function, damage, cause and symptoms of olfactory nerve?

Answer 524

olfaction (smell)

damage causes anosmia (loss of smell) and hyposmia (reduced smell) and calcosmia (smell a bad smell always)

causes by trauma, meningitis, nasal congestion, tumours on floor of anterior fossa

Question 525

Function, damage, cause and symptoms of optic nerve?

Answer 525

for visual acuity, colour vision

damage can cause optic atrophy, visual field defects, blurred vision, scotomata (decreased vision in visual field)

Question 526

What controls papillary responses?

Answer 526

optic and oculomotor nerve

damage caused by ichemia, edema, hemorrhage and trauma

Question 527

What are the 3 main main types of visual field defect and the causes?

Answer 527

monocular - damage to eye or nerve
bitemporal - lesion at chiasm
homonymous hemianopia - lesions in tract, radiation or lesion in visual cortex

Question 528

What does a retinal lesion cause?

Answer 528

paracentral scotoma

Question 529

What does optic nerve lesion cause?

Answer 529

mononuclear field loss (if complete destruction, leads to blindness and loss of pupillary light reflex)

Question 530

What does a chiasmal lesion cause?

Answer 530

bitemporal hemianopia

Question 531

What does an optic tract lesion cause?

Answer 531

homoymous hemianopia (macular involvement)

Question 532

What does a temporal lesion cause?

Answer 532

homoymous quandrantopia (macular involvement)

Question 533

What does a parietal lesion cause?

Answer 533

homonymous quadrantopia (macular involvement)

Question 534

What does a occipital cortex or optic radiation cause?

Answer 534

homoymous hemianopia (macular sparing)

Question 535

What does an occipital pole lesion cause?

Answer 535

homoymous hemianopia (macular sparing)

Question 536

Causes of an optic nerve lesion?

Answer 536

demyelination, nerve compression, occlusion of retinal artery, trauma, papilloedeme, severe anemia, drugs, toxins

Question 537

What causes a defect in the optic chiasm?

Answer 537

pituitary adenoma compressing the decussating fibres from the nasal half of each eye, craniopharyngioma, secondary neoplasm

Question 538

What causes a defect of the optic tract and radiation?

Answer 538

tumour, vascular accident

Question 539

Why is the macular region spared in occipital cortex defects?

Answer 539

in ischemic lesions due to the dual blood supply of this area from the middle and posterior cerebral arteries

Question 540

Symptoms of papiloedema?

Answer 540

disc oedema develops, enlargement of a blind sport and blurring of vision, leading to optic neuritis and visual loss

Question 541

Causes of papilloedema?

Answer 541

raised ICP from tumour, abscess of meningitis, retinal vein obstruction form thrombosis or compression, optic neuritis from demyelination causing inflammation or accelerated hypertension

Question 542

What causes the pupil to constrict?

Answer 542

bright light, stimulates the Edinger-Westphal nucleus in the midbrain (via the optic tract and the convergence centre in the midbrain) and oculommotor nerve causing contriction

Question 543

What causes pupil dilation?

Answer 543

sympathetic fibres in the hypothalamus running through the brainstem into the cervical cord and emerge in the spinal cord at T1 to ascend to the neck

Question 544

Causes of persistent pupillary dilation?

Answer 544

third cranial nerve palsy, antimuscarinic eyedrops, myotonic pupil (Holmes-Adie pupil) which is a delayed/absent reaction to light and convergence seen in young women

Question 545

Causes of persistent pupillary constriction?

Answer 545

parasympathetic eyedrops for glaucoma, Horner’s syndrome, Argyll Robertson pupil, opiate addiction

Question 546

What is Horner’s syndrome?

Answer 546

interruption of the sympathetic fibres to one eye, causing unilateral pupillary constriction, slight ptosis, enophthalmos, loss of sweating on ipsilateral side of the face

Question 547

What is Argyll Robertson pupil?

Answer 547

small irregular pupil fixed to light and contricts on convergence, caused by neruosyphilis and DM

Question 548

Function, damage, cause and symptoms of occulomotor nerve?

Answer 548

control ciliary muscles in the eye, change the shape of the eyes for accommodation for viewing objects

damage can cause dipilopia (double vision), unilater complete ptosis and ocular nerve palsy

causes deviation down and out of the eyes

caused by trauma or berry aneurysm in the posterior communicating artery which runs alongside the nerve

Question 549

Function, damage, cause and symptoms of the trochlear nerve?

Answer 549

Controls extrinsic eye muscles (suoerior oblique muscle)

damage can cause eye problems and vertical diplopia (WHEN LOOKING DOWN OR AWAY FROM AFFECTED SIDE) and nerve palsy (weakness or inability of the nerve)

caused by grave’s disease

Question 550

Function, damage, cause and symptoms of the trigeminal nerve?

Answer 550

for mastication muscles and skin sensation of face and scalp, supplies mucus membranes of sinuses, nose, mouth, tongue and teeth

damage can cause face pain (forehead) and difficulty clenching the jaw, pain when eating, jaw deviates to side of lesion

caused by neurlagia, herpes virus, carcinoma

Question 551

Function, damage, cause and symptoms of the abducens never?

Answer 551

extrinsic eye movement via the lateral rectus muscle

damage causes one eye to face inwards permanently this produces a squint and diplopia when looking at the side of the lesion

caused by nerve palsy, cerebral vascular accidents, combined damage from cranial nerve 4

Question 552

Function, damage, cause and symptoms of facial nerve?

Answer 552

for taste, saliva and tear secretion and facial expression

damage causes lack of facial expression on the affected side of the face (bells palsy), impaired taste

severe damage can cause face paralysis

caused by versticular voster virus and trauma

Question 553

What does 7th nerve palsy, cerebellar signs and 5th, 6th and 8th nerve involvement suggest?

Answer 553

lesion of the cerebellopontine angle, from a meningioma or acoustic neuroma

Question 554

What do cavernous sinus lesions involve?

Answer 554

oculomotor nerves, opthlamic, maxialy division

Question 555

What conditions can affect the cranial nerves?

Answer 555

DM, sarcoidosis, vasculitis, syphilis, brain stem tumours, MS, infarction

Question 556

What is Bell’s palsy and when does it occur?

Answer 556

acute isolater unilateral facial nerve palsy caused by a viral infection (herpes simplex) cause swelling of the 7th nerve within the petrous temporal bone, peak incidence between 65-74 and more common in pregnancy

Question 557

Function, damage, cause and symptoms of vestibulocochlear nerve?

Answer 557

for hearing and vestibular function (balance)

damage can cause sensorineural deafness and tinnitus (noise ringing in ear), veritgo (illusion of movement which can cause vomiting), loss of air conduction in ear, nystagmus and loss of balance

caused by perilymph fistula, cochlear concussion and auditory oscicle disruption and damage to nerve directly

Question 558

What is nystagmus?

Answer 558

rhythmic oscillation of the eyes can be pendular (pendular movement of the eyes, no rapid phase, occurs with poor visual fixation or congental lesion) or jerk (fast and slow component)

Question 559

What is the difference between horizontal and veritical nystagmus?

Answer 559

horzontal can be peripheral (transient minutes or hours) or central lesions (weeks, months)

Question 560

Function, damage, cause and symptoms of the glossopharengeal nerve?

Answer 560

taste, tongue sensation, saliva secretion, o2 and co2 monitoring in blood

damage causes pain in tongue, throat, tonsils and ear from compression of nerve

damage caused by combination to 10 and 11

Question 561

Function, damage, cause and symptoms of vagus nerve?

Answer 561

taste, pharyngeal activity, epiglottis sensation, innervation of GI tract, control trachea and cardiac muscles

damage causes dysphgaia, difficulty speaking, vocal cord weakness, damage to nuclear amygus, cause aphonia (harsh voice), pain

Question 562

Function, damage, cause and symptoms of the accessory nerve?

Answer 562

pharynx, larynx and soft palate muscles, sternocleoidmastoid and trapezius muscles

damage causes paralysis of the sternocleoidmastoid muscle leadness to flatness of neck and inability to rotate the neck, paralysis of trapezius muscle causing drooping of muscle and inability to raise shoulders

damage usually involves nerves 9 and 10, cuased by wound to neck

Question 563

Function, damage, cause and symptoms of the hypoglossal nerve?

Answer 563

for tongue muscles

damage cause lingual paralysis, dysarthria, and dysphagia, muscle tongue atrophy, so half of tongue cannot be controlled and deviates to side of lesion.

caused by tumour, stroke, infection

Question 564

Function of spinal nerves?

Answer 564

carry information between CNS and periphery

Question 565

What are the two pathways that the peripheral ascend to the thalamus and the cerebral cortex?

Answer 565

posterior columns - carrying sensory modalities for vibration, joint position sense, two point discrimination and light touch, they ascend uncrossed to the gracile and cuneate nuclei in the medulla, then the second oder neurons cross the midline to form the medial lemniscus and pass to the thalamus

spinothalamic tracts - carry sensations of pain and temperature, fibres synapse in the dorsal horn of the cord, crossing the midline and ascend as the spinothalamic tracts to the thalamus

Question 566

What are the main symptoms of posterior column and spinothalamic tract lesions?

Answer 566

paraesthesiae, numbness and pain

Question 567

Symptoms of peripheral nerve lesions?

Answer 567

felt in the distribution of the affected peripheral never e.g. median nervem has bilateral symmetrical, distal sensory loss and burning

Question 568

Symptoms of spinal root lesions?

Answer 568

symptoms in the dermatome supplied by that root, tinglign discomfort (if it was a lesion of the sensory tract there would be general symptoms no specific dermatomes

Question 569

Symptoms of spinal cord lesions?

Answer 569

evident below level of lesion

spinothalamic leads to contralateral pain and temperature sensation loss below lesions

proprioception lesion results in loss of this ipsilaterally below lesion

Question 570

Symptoms of a pontine lesion?

Answer 570

loss of all forms of sensation on opposite side of lesion

Question 571

Symptoms of thalamaic lesions?

Answer 571

complete contralateral sensory loss and spontaenous pain (caused by thalamic infarct)

Question 572

Symptoms of cortical lesions?

Answer 572

sensory loss, neglect of one side of the body, subtle disorders of sensation , no pain

Question 573

Upper motor neuron lesion symptoms?

Answer 573

oppssite side to lesion

fasciculation absent, no muscle wasting, spasticity, clonus, weakness in arm extensors and leg flexors, exaggerated tendon reflexes, extensor plantar response, drift of the outstretched hand downwards

Question 574

Lower motor neuron lesion symptoms?

Answer 574

signs are on the same side

fasiculation present, wasting, hypotonia, loss of tendon reflexes

Question 575

What is fasciculation?

Answer 575

visible contraction of single motor units, appearing as a twitch

Question 576

Symptoms of acute injury to upper motor neurons?

Answer 576

transient flaccid weakness and hyporeflexia

Question 577

What are the 2 main patterns of clinical features that occur in UMN disorders?

Answer 577

hemiparesis - weakness of the limbs on one side, usually caused by lesion within brain or brainstem e.g. stroke

paraparesis - weakness of legs, bilateral damage to corticospinal tracts caused by lesions below T1, tetraparesis in quadriplegic, weakness of arms and legs indicating high cervical cord damage from trauma - cord lesions result in UMN signs below lesion, LMN signs at lesion and unaffected muscle above lesion

Question 578

What mainly causes LMN lesions?

Answer 578

anterior horn cell lesions (MND and poliomyelitis)

spinal root lesions (cervical and lumbar disc lesions)

peripheral nerve lesions (trauma, compression, polyneuropathy)

Question 579

Based on rapidity of onset, what does vision loss suggest the cause?

Answer 579

sudden - vascular (GCA)

acute - inflmmatory/infectious (optic neuritis, TB)

subacute - inflammatory/infectious/neoplastic

chronic - neoplastic/degenerative

episodic - migraine

Question 580

Based on symptoms, what is the suggesting cause of vision loss?

Answer 580

headache - migraine, tumour, raised ICP

malaise, fever, myalgia, headache, jaw claudication - giant cell arteritis

painful monocular visual loss - optic neuritis

systemic weakness, dysarthria, dysphagia - MG

dysarthria and ataxia - posterior fossa lesion

Question 581

What social factors could lead to vision loss?

Answer 581

smoking, alcohol - carcnoma and tobacco alcohol amblyopia

diet - nutritional optic neuropathy

occupation

Question 582

What genetic disorders can cause vision loss?

Answer 582

Leber’s herditary optic neruopathy and AD/R optic neuropathy, MS

Question 583

What is the papillomacular bundle?

Answer 583

contains >90% of all retinal nerve fibres in the optic nerve, projecting images from the macula, with a high metabolic activity

lesions causes a central or centro caecal scotoma (lebers hereditary optic neuropathy, toxic and nutritional optic neurpathy and optic neuritis)

Question 584

What causes a superior homonymous quadtrantanopias?

Answer 584

lesion of Meyers loop

inferior striate cortex below the calcarine fissure lesion

Question 585

What causes an inferior homonymous quadrantanopias?

Answer 585

parietal lobe lesions and superior striate cortex lesions

Question 586

What is an incongruous visual field defect?

Answer 586

the defects do not match up between the two eyes

Question 587

When does macular sparing occur?

Answer 587

with occipital lesions that spare the posterolateral striate cortex due to the contralateral blood supply

Question 588

What are the different causes of ptosis?

Answer 588

partial - horners syndrome
complete - third nerve palsy
varying/fatiguing - MG