Deck 3 - neuro

Question 1

Q. What is the papillo-macular bundle? What diseases are associated with it?

Answer 1

A. Contains 90% of retinal nerve fibres in the optic nerve and projects images from

the macula – has high metabolic activity

B. Diseases: optic neuritis, leber’s hereditary optic neuropathy, toxic and nutritional

optic neuropathy – - common in alcoholics

C. Central or centro-caecal syndrome

D. Colour vision loss if often a feature – parvocellular ganglion loss

Question 2

Q. What decussates in the optic chiasm? What would result from a lesiomn here?

Answer 2

A. The nasal retinal fibres – a lesion would result in bitemporal hemianopia

Question 3

Q. What do fibres of Meyer’s loop carry? What do leisons cause?

Answer 3

A. Sweeps back over the temporal lobe, carries superior info

B. Leison: produce superior homonymous quadrantanopias (pie in the sky)

Question 4

Q. What occurs in a trochlear nerve palsy? (CN4)

Answer 4

A. (Innervation of SO – often a congenital palsy) – head tilt (neck pain), hyper

deviation of the L eye that increases right gaze and downgaze

Question 5

Q. What occurs in an abducens nerve palsy?

Answer 5

A. Innervation of lateral rectus muscle – double vision, affected eye is turned in

towards nose

B. Symptoms may be due to false localising sign due to increased CSF pressure

Question 6

Q. What may cause ptosis of the eyelid?

Answer 6

A. Partial ptosis – horner’s syndrome – involvement of muller’s muscle

B. Complete ptosis – third nerve palsy

C. Varying/fatiguing ptosis – myasthenia gravis

Question 7

Name 5 features of the immune system involved in MS pathogenesis

Answer 7

A. T-lymph, B-lymph, macrophages, complement, cytokines

B. Causes demyelination – variable oligodendrocyte loss - ineffective remyelination

can occur

Question 8

Q. Name 5 differences between active and inactive MS

Answer 8

A. Active: demyelination breakdown products present (absent in inactive), hyper

cellular plaque due to infiltration of tissue with inflammatory cells (hypocellular

in inactive), perivenous inflammatory infiltration with mostly macrophages and

T-lymph (variable in inactive state), extensive BBB disruption (mod to minor in
inactive), older active plaques may have central gliosis (in inactive MS the plaques have gliosed)

Question 9

Q. Describe 10 possible symptoms of MS – depending on the site effected

Answer 9

A. Typical: optic neuritis (impaired vision and eye pain), spasiticity and other

pyramidal signs, sensory symptoms and signs, Lhermitte’s sign, nystagmus,

double vision and vertigo, bladder and sexual dysfunction

B. Spinal cord: weakness, paraplegia, spasticity, tingling, numbness, Lhermitte’s sign, bladder and sexual function

C. Cerebral hemispheres: large variety – also many silent features, depression, anxiety, fatigue, cognitive impairment

D. Optic nerves: impaired vision, eye pain

E. Medulla and pons: dysarthria, double vision, vertigo, nystagmus

F. Cerebellar white matter: dysarthria, nystagmus, intention tremor ataxia

Question 10

Q. What are the five most common first symptoms of MS?

Answer 10

Weakness, paraesthesia, visual loss, incoordination, vertigo, sphincter

impairment

Question 11

Q. What investigations could be done for MS?

Answer 11

CT, CSF electrophoresis oligoclonal IgG banding

Question 12

Q. Describe the classes of immunoglobulins

Answer 12

A. IgA: found in mucosal areas: gut, resp, urogenital, saliva, tears, breast milk – prevents colonisation by pathogens

B. IgD: acts as an antigen receptor on B cells – activates basophils, mast cells to produce antimicrobial factors

C. IgE: binds to allergens and triggers histamine release from mast cells and
basophils – allergy

D. IgG: antibody-based immunity (passive immunity to featus)

E. IgM: Expressed on B cells, eliminates pathogens in early stages before there is sufficient IgG

Question 13

Q. What is MS treated with?

Answer 13

A. DMARDS: betaferon (main adverse effects: infection site reactions, flu-like symptom complex, mild lymphopenia, mild rises in liver enzymes)

B. Interferon beta-1b and beta 1a

C. Muscle relaxers - others: baclofen, diazepam, dantrolene, clonidine, tizanidine

D. If focal disabling spasticity – peripheral nerve blocks e.g. phenol, alcohol, botulinum toxin

E. Severe: inthrathecal baclofen, functional neurosurgery

F. Tremor Tx: beta-blockers, low dose barbiturates (e.g. phenobarbitone and primidone), gabapentin, isnoizid also: orthotic devices, thalamic surgery

G. Others: bladder control, bowel dysfunction, sexual dysfunction, depression, anxiety, cognitive dysfunction, fatigue

Question 14

Q. What is epilepsy?

Answer 14

A. Paroxysmal event in which changes of behaviour, sensation or cognitive processes are caused by excessive, hypersynchronous neuronal discharges in the brain.

Question 15

Q. What are the three stages of an epileptic seizures

Answer 15

A. Tonic, rigid, recovery

Question 16

Q. Name 5 features of an epileptic seizure

Answer 16

A. Duration 30-120 seconds

B. Positive ictal symptoms - ltered conciousness e.g. confusion, drowiness,

C. Postictal symptoms - altered conciousness

D. Stereotypical seizures/syndromal seizures types

E. May occur from sleep

F. May be associated with other brain dysfunction

G. Typical seizure phenomena: lateral tongue bite, déjà vu etc

Question 17

17. Q. What is syncope?

Answer 17

A. Paroxysmal event in which changes in behaviour, sensation and cognitive

processes are caused by an insufficient blood or oxygen supply to the brain.

Question 18

Q. Name 5 differentiating features of syncope?

Answer 18

A. Situational

B. Typically, from sitting or standing

C. Rarely from sleep

D. Presyncopal symptoms

E. Duration 5-30 seconds

F. Recovery within 30 seconds

G. Cardiogenic syncope: less warning, history of heart disease

Question 19

Q. What are nonepileptic seizures?

Answer 19

A. Paroxysmal event in which changes in behaviour, sensation and cognitive

function caused by mental processes associated with psychosocial distress.

Question 20

20. Q. Name 5 differentiating features of syncope?

Answer 20

A. Situational

B. Duration 1-20 minutes

C. Dramatic motor phenomena or prolonged atonia

D. Eyes closed

E. Ictal crying and speaking

F. Surprisingly rapid or slow postictal recovery

G. History of psychiatric illness, other somatoform disorders

Question 21

Q. What is focal epilepsy? What is first line tx?

Answer 21

A. Associated with focal brain abnormality, may start at any age. EEG shows

changes in focal seizure. Often associated with aura/smell beforehand

B. Seizure types:

1. Partial seizures with impairment of consciousness (e.g.: Psychomotor

seizures)

2. Partial seizures without impairment of consciousness. (e.g.: Jacksonian

seizures, Déjà vu) –

3. Secondary generalised seizures

C. First line treatment: Carbamazepine or lamotrigine

Question 22

Q. What is idiopathic (primary generalised epilepsy? What is first line tx?

Answer 22

A. No associated brain abnormality, manifestation usually < 30 years

B. Seizure types:

1. Absence seizures (e.g.: childhood absence epilepsy, juvenile absence

epilepsy)

2. Myoclonic seizures (e.g.: in juvenile myoclonic epilepsy)
3. Primary generalised tonic clonic seizures (e.g.: Grand mal on awakening)

C. First line treatment: Valproate or lamotrigine

Question 23

Q. What other treatments are available to treat epilepsy?

Answer 23

A. Epilepsy surgery (vagal nerve stimulator)

Question 24

Q. What type of haemorrhage may be caused by acceleration/deceleration

damage?

Answer 24

A. Subdural haemorrhage – traction of bridging veins

B. Force causes differential movement of skull and brain

C. Causing shearing, traction and compressive stresses – damage of blood vessels

and axons

D. Contusions: cause superficial bruises of the brain “coup” at the site of impact and

“contre coup” away from the site of impact

E. Lacerations: when contusion is sufficient to tear the pia mater

Question 25

Q. What may cause brain swelling?

Answer 25

A. Congestive brain swelling: Vasodilation and ↑ cerebral blood volume

B. Vasogenic oedema: Extravasation of oedema fluid from damaged blood vessels

C. Cytotoxic oedema: Increased water content of neurons and glia

Question 26

Q. What is chronic traumatic encephalopathy?

Answer 26

A. Developed countries: traumatic brain injury associated with loss of consciousness

B. Boxer, American football players

C. Initially irritability, impulsivity, aggression, depression, memory loss

D. Then dementia, gait and speech problems, parkinsonism

E. Some have motor neurone disease-like symptoms

F. Features:

i. atrophy of: neocortex, hippocampus, diencephalon, mammillary bodies
ii. 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 27

Q. Name 4 features of brain stem death

Answer 27

A. Pupils, corneal reflex, caloric vestibular reflex (cold/warm water/air into external auditory canal)