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Clinical Practice > Neurosciences > Flashcards

Neurosciences Flashcards

1
Q

what causes increased tone?

A

UMN - spasticity, velocity dependent, clasp knife

extrapyramidal - velocity independent, cog-wheel

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2
Q

what is the cause of increased and abnormal reflexes?

A

clonus

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3
Q

where is the location of UMN?

A

cerebral cortex
brainstem
spinal cord (myelopathy)

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4
Q

where is the location of LMN?

A 
anterior horn cell
nerve roots (radiculopathy)
peripheral nerve (neuropathy)
nerusomuscular junction
muscle (myopathy)
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5
Q

what are the general UMN signs?

A 
increase tone (clasp-knife feel)
weakness of upper limb extensors and lower limb flexors
increased reflexes
extensor plantar
ankle clonus
Hoffmans sign
no muscle wasting
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6
Q

describe spinal cord UMN weakness

A

absent facial weakness

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7
Q

describe motor cortex UMN weakness

A

facial weakness on the same side as limb weakness

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8
Q

describe brainstem UMN weakness

A

facial weakness on opposite side of limb weakness

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9
Q

describe mid pons UMN weakness

A

jaw jerk

motor component of trigeminal nerve

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10
Q

what are the general LMN signs?

A

muscle wasting
decreased tone
reduced/absent reflexes
flexor plantar

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11
Q

describe anterior horn cell LMN weakness

A

fasciculation

wasting

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12
Q

describe nerve root (radiculopathy) LMN weakness

A

pain
weakness
numbness in a particular myotome/dermatome

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13
Q

describe peripheral nerve (neuropathy) LMN weakness

A

often length dependent (distal becoming proximal)
reflexes lost early
wasting ++
often sensory and autonomic involvement

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14
Q

describe neuromuscular junction LMN weakness

A

fatiguable weakness
no pain
diurnal fluctuation
extra ocular involvement; ophthalmoplegia, ptosis, diplopia
bulbar muscle involvement; chewing, swallowing, nasal speech
most common condition; myasthenia gravis

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15
Q

describe myopathy LMN weakness

A 
often proximal weakness
symmetrical weakness
can be painful
reflexes spared until late
\+/- wasting (late)
may have pseudohypertrophy
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16
Q

describe the dorsal column

A

carriers sensory signals of proprioception and vibration

stays on the same side as the receptor and crosses at the medulla

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17
Q

describe the spinothalamic tracts

A

carries sensory signal of pain, temperature and fine touch

crosses to the opposite site immediately when it enters the spinal cord

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18
Q

describe Guillain-Barre syndrome

A

acute paralytic polyneuropathy
LMN
associated with campylobacter jejuni, cytomegalovirus, epstein barr virus

B cells create antibodies against the antigens on the pathogen
these may target proteins on the myelin sheath of the motor never cell or the nerve axon

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19
Q

what are the symptoms and signs of Guillain-Barre syndrome?

A 
reduced reflexes
symmetrical ascending weakness
peripheral loss of sensation
neuropathic pain
cranial nerve (facial) weakness

symptoms usually start within 4 weeks of the preceding infection

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20
Q

what is the management of Guillain-Barre syndrome?

A

IV immunoglobulins/plasma exchange
supportive care
VTE prophylaxis
respiratory failure - intubation, ventilation, ICU admission

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21
Q

describe posterior spinal cord lesion

A 
dorsal column impairment
intact spinothalamic tracts
flexor muscle weakness in both legs
symmetrical
brisk reflexes
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22
Q

describe a spinal cord lesion affecting the whole cord at about T10

A

increasing difficulty walking over the last few weeks
weakness of the flexor muscles in the legs
brisk reflexes
all sensory modalities impaired in the legs
light touch and pinprick sensation impaired onto the abdomen up to the umbilicus

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23
Q

describe myasthenia gravis

A

neuromuscular junction disorder
autoimmune production of AChR antibodies which bind to the postsynaptic NMJ receptors - less effective stimulation of muscle with increased activity
muscle weakness that gets progressively worse with activity and improves with rest
typically women <40 and men >60
strong link with thymoma

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24
Q

what antibodies are responsible for myasthenia gravis?

A

AChR
MuSK
LRP4

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25
Q

what are the symptoms and signs of myasthenia gravis?

A 
fatiguability; clinical hallmark
diplopia
ptosis
ophthalmoplegia
facial movement weakness
dysphagia
fatigue in the jaw when chewing
slurred speech
neck extension/flexion weakness
proximal limb weakness
finger extensor weakness
no wasting, reflexes or sensory involvement
progressive weakness with repetitive movements
diurnal variation
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26
Q

describe brown sequard syndrome

A

hemisection of half the spinal cord due to injury
ipsilateral side - loss of vibration, motor function, deep touch, position sense
contralateral side - loss of pain, temperature, fine touch

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27
Q

name the primary headaches

A

migraine
tension type
trigeminal autonomic cephalgias

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28
Q

name the secondary headaches

A 
head and neck trauma
cranial or cervical vascular disorders
non-vascular intracranial disorders
a substance or its withdrawal
infection
disorder of homeostasis
disorder of neck, cranium, eyes, ears, nose, sinuses, teeth or mouth
psychiatric disorder
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29
Q

describe the symptoms of a tension type headache

A 
bilateral
pressing/tightening
non-pulsating
mild-moderate pain
lasts 30 minutes
continuous
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30
Q

what is the difference between an episodic or chronic tension type headache or migraine?

A

episodic - <15 days/month

chronic - >15 days/month for over 3 months

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31
Q

describe the symptoms of a migraine

A

unilateral or bilateral
pulsating
moderate-severe pain
photosensitivity, hyperacusis, nausea, vomiting
aura - flickering lights, spots, lines, partial loss of vision, numbness, pins and needles, speech disturbance
lasts up to 72 hours

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32
Q

what are the symptoms of a cluster headache?

A 
unilateral (around the eye, above the eye and along the side of the head/face)
can be sharp, boring, burning, throbbing or tightening
severe-very severe pain
restlessness
agitation
red eye
watery eye
nasal congestion
runny nose
swollen eyelid
forehead and facial sweating
constricted pupil
drooping eyelid
lasts 15-180 minutes
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33
Q

what is the treatment of tension-type headaches?

A

aspirin
paracetamol
NSAID

do not offer opioids

chronic - 10 sessions of acupuncture over 5-8 weeks, amitriptyline 10-75mg

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34
Q

what is the treatment of an episodic migraine?

A

fluids
oral paracetamol 1g, naproxen 250mg, aspirin 900mg, metoclopramide 10mg, voltarol 100mg PR, triptan
IV metoclopramide 10mg, paracetamol 1g, magnesium sulphate 500-1000mg, aspirin 900mg
nerve blocks
realistic expectations

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35
Q

what is the treatment of a chronic migraine?

A 
amitriptyline 10-150mg
propanolol 80-240mg
topiramate 25-100mg
candersartan 4-16mg
pizotifen 0.5-4.5mg

botox - inhibits the release of peripheral nociceptive neurotransmitters, must have failed on 3 preventers
electrical neuromodulation
single-pulse transcranial magnetic stimulation
non-invasive vagus nerve stimulation

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36
Q

describe the features of trigeminal autonomic cephalgias

A 
unilateral
ptosis
conjunctival injection
lacrimation
nasal congestion rhinorrhea
restlessness
severe pain
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37
Q

describe the acute treatment and prevention of a cluster headache

A

acute treatment - sumatriptan sc, high flow oxygen, nerve blocks
prevention - verapamil, topiramate, lithium

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38
Q

what may be the causes of systemic symptoms associated with headaches?

A 
fever
weiht loss
fatigue
HIV
cancer
immunosuppression

infection
inflammation
metastatic cancer
carcinomatous meningitis

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39
Q

what may be the causes of neurologic symptoms/signs with headaches; altered consciousness, focal deficits?

A

encephalitis
mass lesion
stroke

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40
Q

what may be the causes of a thunderclap or abrupt onset of headache?

A

SAH
IPH
RCVS

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41
Q

what may be the cause of a new onset headache >50?

A

temporal arteritis

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42
Q

what may be the cause of a positional headache, prior HA, papilloedema?

A

intracranial hypertension
dysautonomia
cervicogenic headache
posterior fossa pathology

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43
Q

what are the symptoms and risk factors for a SAH?

A

thunderclap headache

female
seizures
vomiting
LOC
focal neurology
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44
Q

what are the secondary causes of a thunderclap headache?

A 
intracerebral or subarachnoid haemorrhage
vertebral dissections
acute hypertension
acute low CSF pressure
cough
micturition
colloid cyst of the third ventricle
reversible cerebral vasoconstrictive syndrome
psychiatric conditions (panic disorder)
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45
Q

what are the causes of meningitis?

A 
bacterial
viral
fungal
rickettsial (Rocky Mountain spotted fever)
parasitic
protozoal
cancer
physical injury
certain drugs (NSAIDs)
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46
Q

what are the symptoms and signs of meningitis?

A 
mild fever
headache with sensitivity to light/sound
stiff neck
loss of appetite
muscle aches
kernig's and brudzinski sign
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47
Q

what are the symptoms and signs of a cervical artery dissection?

A 
headache
ataxia
vertigo
vomiting
numbness on one side of face
horner's syndrome
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48
Q

describe a headache caused by a brain tumour

A

<1% of patients have only headache
pain worse with valsalva manoeuvre, exertion, bending over
often awaken from sleep

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49
Q

describe the intracranial compartments

A

supratentorial - frontal, temporal, parietal, occipital lobes, hypothalamus, thalamus
infratentorial - brainstem (midbrain, pons, medulla), cerebellum

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50
Q

describe the craniospinofluid pathways

A

ventricular system

subarachnoid space

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51
Q

what are the functions of the frontal lobe?

A 
motor function
speech
high cognitive function
micturition
personality
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52
Q

what are the functions of the parietal lobe?

A

sensory awareness
spatial awareness
visual tracts

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53
Q

what are the functions of the temporal lobe?

A

vision
receptive speech
memory

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54
Q

what is the primary function of the occipital lobe?

A

vision

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55
Q

what is the primary function of the cerebellum?

A

coordination

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56
Q

what is normal ICP in the resting state?

A

10mmHg

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57
Q

describe an extradural haematoma

A

high density biconcave shape adjacent to the skull
often associated with a lucid interval between initial impact and onset of neurological deterioration
can be caused by focal trauma
good prognosis

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58
Q

describe a subdural haematoma

A

crescentic mass of increased attenuation adjacent to inner table of the skull
rotational movement and tearing of the bridging veins between the brain and the dura

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59
Q

describe skull fractures

A

open - scalp laceration
depressed - lies below adjacent bone
comminuted - multiple fragments

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60
Q

describe gliomas

A

tumours of glial cell; astrocytoma, oligodendroglioma, ependymoma
median survival 1 year following resection, radiotherapy and chemotherapy

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61
Q

describe meningiomas

A

arise from meninges (arachnoid)
primary goal - surgical excision
recurrence - repeat surgery or radiation

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62
Q

describe pituitary adenomas

A

macro and microadenomas

compression of adjacent structures; optic nerve (bitemporal hemianopia)

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63
Q

name some examples of pituitary microadenomas

A

prolactinoma
GH-secreting (acromegaly)
ACTH (Cushing’s)

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64
Q

define a vestibular schwannoma

A

slow-growing benign nerve sheath tumours arising on the vestibular nerve

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65
Q

what are the symptoms and signs of a vestibular schwannoma

A

hearing loss
tinnitus
balance problems

associated with neurofibromatosis

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66
Q

describe stereotactic radiosurgery

A

use stereotactic localisation to precisely focus a large dose of radiation onto a lesion, usually in a single treatment

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67
Q

define hydrocephalus

A

imbalance in the normal CSF production vs resorption process

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68
Q

describe communicating hydrocephalus

A

CSF circulation blocked at the level of arachnoid granulations
4th ventricle open
CSF malabsorption

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69
Q

describe obstructive/non-communicating hydrocephalus

A

blockage proximal to arachnoid granulations
enlargement of ventricles proximal to blockage
e.g. posterior fossa tumour

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70
Q

what is the treatment of hydrocephalus?

A

ventriculoperitoneal shunt

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71
Q

what is the treatment of a cerebral aneurysm?

A

endovascular occlusion using coils

open surgical approach of applying a clip across the aneurysm neck

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72
Q

define an arteriovenous malformation

A

an abnormal collection of blood vessels wherein arterial blood flows directly into draining veins without the normal interposed capillary beds
causes an intraventricular bleed

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73
Q

what is the treatment of arteriovenous malformation?

A

surgery
embolisation
stereotactic radiosurgery

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74
Q

what are the risk factors and symptoms of intracranial infection?

A

previous trauma
recurrent sinus infection
infected heart valves
poor dental hygiene

headache
drowsiness
seizures
fever

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75
Q

what are the pathologies of intracranial infection?

A

meningitis
brain abscess
subdural empyema

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76
Q

what is the treatment of intracranial infection?

A

urgent surgical drainage/evacuation
prolonged course of antibiotics
regular clinical, serological and imaging surveillance until infection resolves

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77
Q

define cauda equina syndrome

A

neurosurgical emergency due to sphincter dysfunction

compression of nerve roots in lumbosacral spine

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78
Q

what are the symptoms and signs of cauda equina syndrome?

A 
radicular pain
parasthesia
weakness
perianal numbness
bladder and sphincter disturbance
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79
Q

what are the underlying pathologies of cauda equina syndrome?

A

tumours
degenerative disease
infection
trauma

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80
Q

define epilepsy

A

a chronic disease of the brain associated with 1 of the following;
> 2 unprovoked seizures >24hrs apart
a single unprovoked seizure with a >60% chance of having another within 10yrs
a diagnosed epilepsy syndrome

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81
Q

describe genetic, primary, or idiopathic epilepsy

A 
known or presumed genetic etiology
associated with;
childhood onset
good response to AEDs
favourable prognosis
"normal brain"
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82
Q

describe structural/metabolic, secondary or symptomatic epilepsy

A 
caused by a distinct structural or metabolic condition
associated with;
onset at any age
variable response to AEDs
variable prognosis
brain pathology
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83
Q

describe focal-onset seizures

A

originate within networks limited to one hemisphere of the brain
may be discretely localised or widely distributed
can be describe as dyscognitive
can evolve to bilateral, convulsive seizures

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84
Q

describe generalised-onset seizures

A

originate at some point with and rapidly engage bilaterally distributed networks
can include cortical and subcortical structures but no the entire cortex
can present as tonic, clonic, tonic-clonic, myoclonic, absences, atonic

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85
Q

describe generalised tonic clonic seizures

A

start with a sudden loss of consciousness
generalised stiffening of the body (tonic)
followed by muscle contraction (clonic)

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86
Q

describe absence seizures

A 
usually during childhood or adolescence
momentary loss of consciousness 3-15s
brief staring spells
eyelid flutter
often undetected
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87
Q

describe myoclonic seizures

A

starts in adolescence and persists throughout adulthood
sudden, brief arrhythmic jerks of arms and other extremities
associated with a fall
no loss of consciousness
shortly after awakening
may be triggered by photic or sensory stimulation or sleep deprivation

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88
Q

what is the treatment of juvenile myoclonic epilepsy?

A

1st line sodium valproate

consider lamotrigine, levetiracetam, topiramate if sodium valproate is unsuitable or not tolerated

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89
Q

define status epilepticus

A 
continuous or rapidly repeating seizures
abnormally prolonged
consider if seizures >5mins
or
2 discrete seizures with no regaining of consciousness inbetween
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90
Q

what is the treatment of status epilepticus?

A

0-10 mins; ABCDE, oxygen

1-60 mins; monitoring, emergency AED, IV lines, investigation, glucose and thiamine?, treatment of acidosis?

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91
Q

what is the treatment of convulsive status epilepticus?

A 
early status (0-10/30mins); lorazepam 0.07mg/kg, repeated once after 20mins
established status (10/30-60/120mins); phenytoin 20mg/kg at 50mg/min
refractory status; general anaesthetic with either propofol, midazalom or thiopentone
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92
Q

define MS

A

chronic, immune mediated, inflammatory, demyelinating disease of theCNS
clinical and radiological episodes occurring over time

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93
Q

what are the risk factors for developing MS?

A 
EBV
genetics
smoking
obesity
female
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94
Q

what are the functions of astrocytes?

A

secretion and absorption of neurotransmitters
maintenance of the blood-brain barrier
nutritional and metabolic support

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95
Q

describe the pathogenesis of MS

A

inflammation
demyelination
axonal injury and neurodegeneration

incomplete remyelination
demyelinating ability decreased with age

brain atrophy
meningeal inflammation
cortical demyelination

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96
Q

what are the consequences of increased meningeal inflammation and cortical demyelination?

A 
more severe disease course
more rapid decline in cognitive function
accumulation of disability
younger age of death
enter progressive stages sooner
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97
Q

what are the features of an MS relapse?

A

an episode of new symptoms or a worsening of an existing MS symptoms over days/weeks
usually followed by in/complete recovery over weeks/months

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98
Q

what are the common symptoms of MS?

A 
weakness
sensory symptoms
visual loss
incoordination
vertigo
bladder; frequency, urgency, incontinence
bowels; constipation, urgency, incontinence
fatigue
pins and needles
neuropathic pain
sexual dysfunction
depression
anxiety
cognitive deficits
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99
Q

what are the common clinical presentations in RRMS?

A

optic neuritis
transverse myelitis
brainstem symptoms

differentiated in time and space

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100
Q

describe the signs and symptoms of optic neuritis

A

unilateral visual (acuity) loss
loss of colour vision
retrobulbar eye pain, exacerbated on eye movement
develops over days and starts to improve within 2 weeks
papilloedema
afferent pupillary defect (dilation rather than constriction)
optic atrophy

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101
Q

describe the signs and symptoms of transverse myelitis

A

area of inflammation within the spinal cord
evolution of symptoms over days
weakness
sensory symptoms
bladder/bowel symptoms
Lhermitte’s phenomenon; electric shock sensation down spine on neck flexion (cervical cord lesion)

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102
Q

describe brainstem symptoms

A 
internuclear ophthalmoplegia (INO); failure of eye adduction, lesion in medial longitudinal fasciculus
diplopia
vertigo
facial/limb weakness/sensory loss
trigeminal neuralgia
nystagmus
ataxia
dysarthria
dysphagia
cranial nerve palsies
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103
Q

what investigations are performed to diagnose MS?

A

blood tests; exclude other neuroinflammatory conditions (ANA, dsANA, anti-cardiolipin, ACE)
CSF; unmatched oligoclonal bands, not MS specific
MRI; typically juxtacortical, periventricular, infratentorial, spinal cord
VERs; delayed in optic neuritis

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104
Q

what are the aims of MS treatment?

A

prevention of relapses
slowing rate of accumulating disability
treatment of an acute relapse
symptomatic treatment of fatigue, neuropathic pain, bladder/bowel dysfunction etc.

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105
Q

what are the disease modifying treatments of RRMS?

A

active - interferon beta, glatiramer acetate, peginterferon beta
highly active - natalizumab, ocrelizumab, alemtuzumab, cladribine

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106
Q

describe the treatment approaches for progressive MS

A

targeting T and B lymphocytes; ocrelizumab, rituximab
mitochondrion protective strategies; minocycline, chelating drugs, antioxidants
anti-inflammatory strategies; riluzole, memantine, amantadine, siponimod, minocycline

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107
Q

describe some of the treatment approaches for CNS remyelination

A 
amiloride at ASIC1
lamotrigine at Na channels
opicinumab at LINGO1
domeperidone at PRLR
clementine, benztropine and quetiapine at M1
vitamin D at VDR
clobetasol at GR
liothyronine at THR
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108
Q

describe polyneuropathies

A 
longest nerves affected first (distal)
symmetrical
weakness +/- sensory loss
reflexes absent
distal wasting
pes cavus
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109
Q

describe motor neurone disease

A

degeneration of cortical pyramidal cells, cortico-spinal pathways, brainstem motor nuclei (V, VII, X, XII) and anterior horn cells
painless progressive weakness and wasting
normal eye movements
normal sensation

combination of UMN and LMN signs

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110
Q

describe fasciculations

A

spontaneous firing os a single motor unit
active denervation
usually MND or a very proximal nerve lesion
can be benign; physical, psychological stress, caffeine

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111
Q

describe mononeuropathy

A

weakness affecting one nerve’s muscles

sensory loss affecting one nerve

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112
Q

describe peripheral neuropathy

A

absent/reduced reflexes
distal, symmetrical sensory loss
foot drop, high steppage gait

e.g. Charcot marie tooth

113
Q

describe MND findings

A

increased reflexes despite other LMN signs

no sensory loss

114
Q

describe myopathy

A

reduced/normal reflexes
no sensory loss
trendelenburg/waddling gait
symmetrical proximal weakness

115
Q

what are the causes of high CK?

A 
black/male
post-high intensity exercise
rhabdomyolysis
muscular dystrophy
denervation
sepsis
renal failure
malignancy
116
Q

what LMN disorders do not have sensory loss?

A

myopathy
MND
myasthenia

117
Q

what are the signs and symptoms of Charcot Marie tooth disease?

A 
pes cavus
distal muscle wasting; champagne bottle
weakness of lower legs
weakness of hands
reduced tendon reflexes
reduced muscle tone
peripheral sensory loss
118
Q

what are the causes of Charcot Marie tooth disease?

A

genetic

alcohol
B12 deficiency
cancer and CKD
diabetes and drugs (isoniazid, amiodarone, cisplatin)
every vasculitis
119
Q

what are the symptoms and signs of amyotrophic lateral sclerosis?

A 
cognitive and behavioural impairment
dysphagia
dysarthria
respiratory insufficiency
muscle cramps
spasticity
muscle weakness and atrophy

motor neurone disease

120
Q

what are the acquired causes of myopathy?

A

autoimmune
endocrine; thyroid, parathyroid, Addison’s, cushing’s
toxic; corticosteroids, colchicine, chloroquine, alcohol, statins
viral; HIV, HCV, influenza
metabolic; Ca2+/K+
critical illness myopathy

121
Q

describe dermatomyositis

A 
inflammatory myopathy
gottron papules
periorbital oedema
heliotrope rash
V sign
shawl sign
mechanics hands
acute/subacute proximal weakness
myalgia
CK 10-50 x normal
associated with malignancy; lung, breast, ovarian, lymphoma
perifascicular and perimysial atrophy on biopsy
122
Q

what is the treatment of dermatomyositis?

A

oral prednisolone 0.5-1 mg/kg/day
acute and severe - IVMP for 3-5 days
long-term immunosuppressants, used in parallel with steroids; methotrexate, azathioprine, mycophenolate
if not tolerated/effective; IVIG, ciclosporin
3rd line; rituximab, cyclophosphamide

123
Q

describe inclusion body myositis

A

late onset progressive myopathy (50-60yrs)
chronic
sporadic
cause unknown
m>f
usually wheelchair use within 10yrs of onset
does not affect life expectancy

124
Q

what are the symptoms and signs of inclusion body myositis?

A 
predominantly proximal weakness and wasting
symmetrical
reflexes spare
some thigh atrophy
dysphagia common (aspiration pneumonia)
no response to steroids
CK increased but <12x normal

biopsy; endomysial inflammatory infiltrates, partial invasion of fibres, rimmed vacuoles. amyloid deposits on electron microscopy

125
Q

what are the causes of neuromuscular junction dysfunction?

A 
myasthenia gravis
Lambert eaton myasthenia syndrome
organophosphate poisoning
botulinum toxin
congenital myasthenic syndromes
126
Q

describe myasthenia gravis

A

autoimmune disorder affecting NMJ
80% AChR antibodies
10-15% MuSK antibodies
5-10% double seronegative MG

degradation and endocytosis of AChRs, degeneration of the motor end-plate and loss of postsynaptic folds
reduced muscle membrane depolarisation
increased in the action potential threshold

127
Q

what are the clinical features of myasthenia gravis?

A 
young women and old men
fatiguability
diurnal variation; fluctuating nature
ptosis
ophthalmoplegia
neck extension/flexion weakness
proximal limb weakness
finger extensor weakness
no wasting
reflexes preserved
no sensory involvement
128
Q

what investigations are required to diagnose myasthenia gravis?

A

AChR antibody
MuSK antibody
ice pack test
tensilon test
edrophonium IV; assess objective improvement in muscle strength
neurophysiology; repetitive nerve stimulation, single fibre EMG
CT chest; exclude thymoma

129
Q

what is the management of myasthenia gravis?

A 
pyridostigmine
steroids
steroid-sparing agents; azathioprine, ciclosporin, methotrexate
IVIg
plasmapheresis (PLEX)
rituximab
130
Q

what factors exacerbate myasthenia gravis?

A 
infection
stress; trauma, post-operative
cholinesterase inhibitors withdrawal
rapid introduction/increase of steroids
electrolyte imbalance
anaemia
antibiotics
penicillamine
anaesthetic agents
quinidine
beta blockers
calcium channel blockers
lithium
chlorpromazine
phenytoin
botox
chemotherapy; cisplatin
131
Q

describe myasthenia crisis

A 
increasing muscle weakness
diplopia
respiratory failure
oxygen saturation and blood gases can be normal until later
FVC; >1L or 15ml/kg requires ICU support
132
Q

what is the management of myasthenia crisis?

A

IVIg or plasma exchange
ventilatory support
NBM
NG feeding

133
Q

define polyneuropathies

A

length dependent (distal( symmetrical weakness/sensory loss

134
Q

what is the differential diagnosis of polyneuropathy?

A 
diabetes
vitamin deficiencies (copper, B12, D, E)
hyper/hypothyroidism
toxins, lead, nitrous oxide
drugs; cisplatin
hereditary
infectious; HIV, EBV, CMV, lyme disease
inflammatory SLE, sjogren's, behcet's
paraneoplastic; myeloma, MGUS
acute/chronic immune demyelination polyneuropathy
135
Q

define Guillain Barre syndrome

A

acute inflammatory demyelinating polyneuropathy

136
Q

what are the triggers for developing Guillain barre syndrome?

A

CMV
mycoplasma pneumoniae
campylobacter jejuni

137
Q

what are the clinical features of GBS?

A 
progressive weakness; hours-days
areflexia
peak <4 weeks
relatively symmetrical
motor - sensory involvement
pain
autonomic dysfunction
facial involvement
bulbar
138
Q

what investigations are required to diagnose GBS?

A 
CSF; increased protein
NCS; demyelination
MRI spine; rule out structural cause
CK; rule out muscle disease
TFTs
K
bone
B12
folate
139
Q

what is the treatment of GBS?

A 
discuss with neurology
IVIG/PLEX
supportive care with airway support
MDT; SALT, physio
enoxaparin
nursing care

10% mortality; neuromuscular respiratory failure

140
Q

define Charcot marie tooth disease

A

general term for a group of inherited sensorimotor neuropathies
dominant (CMT1A), recessive or X-linked

141
Q

what are the clinical features of Charcot Marie tooth disease?

A

gradual, progressive, length dependent weakness and wasting
foot deformity; from childhood, pes cavus
Champagne bottle deformity
upper limb involvement eventually
no cardiac or respiratory involvement
no current treatment

142
Q

describe motor neurone disease

A

fatal degenerative condition
degeneration of cortical pyramidal cells, corticosteroids-spinal pathways, brainstem motor nuclei (V, VII, X, XII) and anterior horn cells

143
Q

what are the subtypes of MND?

A

amyotrophic lateral sclerosis; most common, mixture of UMN and LMN signs
progressive muscular atrophy; LMN signs only
progressive bulbar palsy; bulbar dysfunction
primary lateral sclerosis; UMN signs only

144
Q

what are the clinical features of MND?

A 
pain progressive weakness and wasting
normal eye movements
jaw weakness
brisk jaw jerk
focal weakness
gag reduced/exaggerated
bulbar/pseudobulbar palsy; bad prognostic sign
tongue fasciculations
head drop
limbs UMN/LMN; triceps weak and wasted, fasciculations, brisk reflex
cachexia
normal sensation
cognition; frontal involvement
145
Q

what is the differential diagnosis of MND?

A

multifocal motor neuropathy
cervical myeloradiculopathy
MG; MND has no ocular involvement
inherited motor neuropathies; MND more rapidly progressive

146
Q

what investigations are required to diagnose MND?

A 
MRI spine
nerve conduction studies
electromyography
exclude metabolic, endocrine, infectious causes
AChR antibodies
genetic testing; FHx
147
Q

what is the management of MND?

A 
SALT
nurse specialist
PEG/RIG; gastroenterology, dietician
NIV; respiratory
palliative; symptom control
riluzole
148
Q

describe the lateral cord of the median nerve

A

made up of C6-7 fibres
sensation; thenar eminence, thumb, index and middle fingers
motor; proximal median muscles of the forearm

149
Q

describe the medial cord of the median nerve

A

made up of C8-T1 fibres
sensation; lateral 1/2 of ring finger
motor; median muscles of distal forearm and hand

150
Q

describe carpal tunnel syndrome

A

most common entrapment neuropathy
f>m

C6-7 nerve root lesion
brachial plexus lesion
proximal median nerve lesion

151
Q

what are the symptoms and signs of carpal tunnel syndrome?

A 
paraesthesia in the median distribution
worse on wakening
motor symptoms
loss of dexterity
55-65% bilateral on first presentation
mostly dominant hand more severely affected
152
Q

what are the risk factors for developing carpal tunnel syndrome?

A 
small carpal tunnel
sex
fractures
DM
inflammatory conditions; RA
hypothyroidism
renal disorders
occupational
153
Q

what are the findings on an examination on a patient with carpal tunnel syndrome?

A

thenar eminence may be spared; innervation from the palmar cutaneous sensory branch
positive tinels and phalens test
wasting of thenar eminence
weakness of thumb abduction and opposition

154
Q

what is the differential diagnosis of carpal tunnel syndrome?

A 
C6/7 root lesion
brachial plexus lesion
proximal median nerve
PN
MND
155
Q

what are the clinical features of C6-7 nerve lesion?

A

reduced reflexes
reduced power; EF, EE, arm pronation
reduced sensation in palm and forearm

156
Q

what are the clinical features of a brachial plexus lesion?

A

similar weakness to cervical radiculopathy
more widespread weakness
reflex changes

157
Q

what are the clinical features of a proximal median nerve lesion?

A

very uncommon

weakness of proximal muscles; distal thumb flexion, arm pronation, WF

158
Q

what does the anterior interosseous nerve supply?

A

motor; flexor policus longus, flexor digitorum profundus (digits 2 and 3), pronator quadratus
sensory; deep sensory fibres to wrist and interosseous membrame

159
Q

what are the causes of anterior interosseous neuropathy (AIN)?

A

fracture mid-shaft of radius
penetrating injury to forearm
excessive exercise
brachial neuritis

160
Q

describe the pathway of the ulnar nerve

A

C8-T1 roots
enters the ulnar groove between medial epicondyle and olecranon process
travels under the two heads of flexor carpi ulnaris muscle

161
Q

what are the clinical features of ulnar neuropathy at the elbow?

A 
decreased grip and pinch
hypothenar eminence atrophy
intrinsic muscles of hand atrophy
wartenberg's sign; abducted 5th finger
benediction posture sign
sensory deficits on ulnar side
162
Q

what is the differential diagnosis of ulnar neuropathy?

A

C8/T1 radiculopathy
lower trunk brachial plexopathy
PN
MND

163
Q

what are the clinical features of C8-T1 cervical radiculopathy?

A

sensory disturbance into forearm

weakness involving APB

164
Q

what are the clinical features of peripheral neuropathy?

A

bilateral wasting
lower limbs
PMHx DM

165
Q

what are the causes of a wrist drop?

A 
CNS lesion
C7/8 radiculopathy
brachial plexopathy
spiral groove
PIN
166
Q

describe the radial nerve

A

receives innervation from all 3 trunks

innervates; triceps, brachioradialis, long head extensor carpi radials, supinator

167
Q

what are the clinical features of radial neuropathy?

A 
wrist and finger drop
mild weakness supination
mild weakness EF
EE spared
ulnar power reduced
sensory disturbance on lateral dorsum of hand
168
Q

what are the causes of radial nerve palsy?

A

Saturday night palsy

humeral fracture

169
Q

what are the clinical features of axillary nerve palsy?

A

tricep involvement; EE weakness
wrist drop
supinator weakness
sensory loss in the distribution of proximal cutaneous branches

170
Q

define parkinsonism

A

the combination of bradykinesia, rigidity and impaired motor control

171
Q

define hemidallismus

A

flinging movements

172
Q

define dyskinesia

A

involuntary movement

fragmentary/incomplete

173
Q

define dystonia

A

prolonged spasms of muscle contraction

174
Q

define akathisia

A

unpleasant sensation of restlessness

inability to sit still or remain motionless

175
Q

what are the hypo kinetic movement disorders?

A

akinetic rigid syndrome
idiopathic Parkinson’s disease
atypical Parkinsonism; MSA, PSP, CBD
drug-induced Parkinsonism

176
Q

what are the hyperkinetic movement disorders?

A 
dyskinesias
essential tremor
dystonia
chorea
hemiballismus
tics
myoclonus
drug-induced dyskinesias
177
Q

describe the pathophysiology of PD

A

loss of dopamine containing neurones result in a pre-synaptic dopaminergic deficit
presence of lewy bodies composed of abnormal protein deposits
loss of pigmented neurones in the substantial nigra

178
Q

what are the clinical features of Parkinson’s disease?

A 
tremor
rigidity
brady/akinesia
postural instability
trembling of head and extremities
forward tilt of trunk
reduced arm swinging
shuffling gait
short steps
no weakness; extrapyramidal disorder
179
Q

describe the tremor of Parkinson’s and how it is examined

A 
pill rolling
reduces on action
increases when distracted/stressed
re-emergent
initially unilateral
jaw, eyelid, chin, foot; suggestive of PD
head tremor; uncommon in PD

hands in lap
outstretched
in front of face
finger-to-nose

180
Q

describe the rigidity of Parkinson’s and how it is examined

A 
stiffness through a range of movement; EF, EE
like a lead pipe
clasp knife
usually asymmetrical
\+ tremor = cogwheel rigidity

at wrist, elbow and other joints

181
Q

describe the akinesia of Parkinson’s and how it is examined

A

decrement in amplitude of repetitive movement
mask-like facies
reduced spontaneous blinking
lack of arm swing

finger taps
playing piano
heel taps

182
Q

describe the postural instability of Parkinson’s and how it is examined

A

sitting; motionless, slumped to one side
gait; stopped/bent, flexed at hips, shuffling steps
positive pull test
falls ‘en bloc’

able to stand with arms crossed
gait
pull test

183
Q

define atypical parkinsonism

A

Parkinsonism + additional features which distinguish them from Parkinson’s disease;
MSA
PSP
CBS

184
Q

what are the clinical features of multiple system atrophy (MSA)?

A 
parkinsonism
ataxia/unsteadiness; cerebellar degeneration
autonomic failure; postural hypotension, impotence, urinary frequency, urgency, incontinence
stridor
sleep breathing problems
jerky postural tremor
high pitched quivering dysarthria
polyminimyoclonus
disproportionate anterocollis
UMN signs
deep involuntary sighs or gasps
185
Q

what is the treatment of multiple system atrophy (MSA)?

A 
symptomatic management only
physio
OT
SALT
BP treatment
186
Q

what are the clinical features of progressive supranuclear palsy (PSP)?

A 
Parkinsonism; symmetrical
atremulous
early falls; classically backwards
axial rigidity; severe neck stiffness
inability to move eyes vertically; staring
pseudobulbar palsy
dementia; frontal lobe
187
Q

what are the clinical features and treatment of progressive supra nuclear palsy (PSP)?

A

loss of balance
falls
slurred speech
difficulty swallowing

amantadine; may improve symptoms

188
Q

what are the clinical features corticobasal degeneration (CBD)?

A 
parkinsonism
alien limb phenomenon
apraxia
myoclonus
dementia
189
Q

what are the causes, clinical features and treatment of drug-induced Parkinsonism?

A

dopamine antagonists; haloperidol, maxolon, metoclopramide, stemetil, prochlorperazine

parkinsonisan syndrome
slowness
rigidity
tremor; less often

stop offending drug
poor response to L-dopa

190
Q

describe an essential tremor

A 
rhythmic oscillation of body part
common
often inherited; AD
slowly progressive
fairly symmetrical
flexion-extension
voice
worse with anxiety, stress, beta agonists
improves with alcohol, beta blockers
shaky handwriting
191
Q

describe dystonia

A

involuntary sustained contractions of opposing muscle groups
twisting movements
abnormal postures

192
Q

what is the clinical presentation of dystonia?

A

abnormal posture
pain
cramps
may be associated with tremor

193
Q

describe adductor and abductor laryngeal dystonia

A

adductor; vocal cords slam together and stiffen, speech sounds strangled, words cut off
abductor; cords fold open and do not vibrate, weak and breathy voice

194
Q

what is the diagnosis and treatment of laryngeal dystonia?

A

laryngoscopy

botulinum toxin injections

195
Q

describe generalised dystonia

A 
primary dystonia
onset <25yrs
typically lower limb onset
50% have DYT1 mutation; AD
craniocervical onset; DYT6
196
Q

describe chorea

A

rapid jerky movement that flit from one part of the body to another
often generalised
may be confined to one body part

197
Q

what are the causes and treatment of chorea?

A

huntington’s disease
rheumatic fever; sydenham’s chorea
drugs; OCP, L-dopa
pregnancy

dopamine receptor blockers; tetrabenazine

198
Q

describe the pathology and clinical features of huntingtons disease

A

loss of nerve cells in caudate nucleus and putamen
reduction in neurotransmitter GABA

inherited progressive chorea
behavioural disturbance
dementia
jerky uncontrollable movements
unsteady gait
difficulty with speech, chewing, swallowing
anxiety
depression
insomnia
199
Q

what is the treatment and prognosis of Huntington’s disease?

A

none to cure/slow the disease
tetrabenzine; reduce chorea

steady progression of chorea and dementia
death; 10-20yrs after onset

200
Q

describe the clinical features, causes and treatment of hemiballismus

A

severe proximal chorea; violent flinging movement of one side of the body
causes; infarction, haemorrhage in the contralateral sub thalamic nucleus
treatment; may settle spontaneously, dopamine blockers, surgery

201
Q

what are the primary causes of tics?

A

simple transient tics of childhood

gilles de la Tourette’s syndrome

202
Q

what are the secondary causes of tics?

A

neurodegenerative disease; HD, wilsons
learning disabilities; Down’s syndrome, rett’s syndrome, autism
infection; Sydenham’s, chorea, PANDAS

203
Q

describe myoclonus

A

brief involuntary twitch of a muscle or group of muscles
may be a normal physiological symptoms; hypnic jerks, hiccups
feature in Parkinson’s disease, epilepsy, CJD
contraction; positive
relaxation; negative

204
Q

what are the causes of drug-induced dyskinesia?

A

levodopa in parkinsons patients
neuroleptic/anti-psychotic medication
tremor; salbutamol, lithium, valproate

205
Q

what are the clinical features of drug-induced dyskinesia?

A

tardive; mouthing, smacking of lips, grimaces with contortion of face and neck, after several years of neuroleptics
acute dystonic reactions; spasmodic torticollis, trismus, oculogyric crises
akathisia

206
Q

how is a parkinsonian syndrome diagnosed?

A

bradykinesia + at least one;
muscular rigidity
4-6 Hz rest tremor
postural instability

207
Q

define bradykinesia

A

slowness of initiation of voluntary movement with progressive reduction in speed and amplitude of repetitive movements

208
Q

describe the gait of Parkinson’s disease

A 
reduced arm swing
reduced stride length and foot lift
clock face or en-bloc turning
narrow base
gait freezing
postural instability; pull test
209
Q

what are the non-degenerative causes of Parkinsonism-like symptoms?

A 
repeated strokes or head injury
Hx of encephalitis
metoclopramide
prochlorperazine
lithium
calcium channel blockers
valproate
210
Q

what are the red flags for degenerative atypical parkinsonian disorders (MSA, PSP, CBD)?

A 
poor/unsustained levodopa response
early recurrent falls
early speech/swallowing difficulty
early cognitive decline
cerebellar, pyramidal signs, dyspraxia or supra nuclear gas palsy
early autonomic dysfunction
211
Q

which neurological diseases have a normal DAT (dopamine transporter) scan?

A 
essential tremor
drug induced Parkinsonism
dystonic tremor
vascular Parkinsonism
dopa-responsive dystona
psychogenic
alzheimer's
FXTAS
212
Q

which neurological disease have an abnormal DAT scan?

A 
parkinson's disease
MSA
PSP
dementia with LBs
CBD
wilson's disease
spinocerebellar ataxia
213
Q

what are the supportive criteria for Parkinson’s disease?

A

> 3 for clinically definite PD

unilateral onset
persistent asymmetry
rest tremor
progressive
excellent levodopa response
levodopa induced dyskinesia
>5yr levodopa response
visual hallucinations
clinical course >10yrs
214
Q

describe the presentation of focal onset seizures

A

with preserved awareness or with impaired awareness

215
Q

describe the effects of a focal onset seizure

A 
focal tonic-clonic limb movements
adverse/contraversive movements
grimacing
autonomic
auditory
visual
somatosensory
216
Q

what is the treatment of generalised tonic-clonic seizures

A

1st line; lamotrigine, levetiracetam, sodium valproate

2nd line; lacosamide, zonisamide, brivaracetam, topiramate, phenytoin, carbamazepine

217
Q

what is the treatment of focal seizures?

A

1st line; lamotrigine, levetiracetam, carbamazepine, sodium valproate
2nd line; zonisamdide, gabapentin, oxcarbazepine, topiramate, phenytoin

218
Q

what is the treatment of absence seizures?

A

1st line; ethosuximide, sodium valproate

2nd line; lamotrigine, clonazepam

219
Q

what are the side effects of levetiracetam?

A

irritability/behaviour change
somnolence
headache

220
Q

what are the sides effects of lamotrigine?

A

rash
stevens-johnson syndrome
toxic epidermal necrolysis (especially in children)
insomnia

221
Q

what are the side effects of carbamazepine?

A

agranulocytosis
SIADH
OP
stevens-johnson syndrome

222
Q

what are the side effects of sodium valproate?

A 
hepatotoxicity
highly teratogenic
weight gain
pancreatitis
thrombocytopenia
223
Q

what are the side effects of phenytoin?

A 
teratogenicity
hirsutism
weight gain
peripheral neuropathy
gum hypertrophy
224
Q

what are the side effects of topiramate?

A 
cognitive problems
speech disturbance
behavioural abnormalities
kidney stones
weight loss
225
Q

describe the clinical features of epilepsy

A 
tonic/clonic motor activity
synchronous limb movements
eyes usually open
pupillary reflexes may be absent
usually <90s
possible injury
tongue bitten high, deep and lateral
1-30mins to reorientation
incontinence common
226
Q

describe the clinical features of syncope

A 
often no movement
multifocal synchronous limb movements
eyes usually open
intact pupillary response
usually <60s
seconds-minutes to reorientation
227
Q

describe the clinical features of NEAD

A 
rhythmical tremulous movement, thrashing/violent
pelvic thrusting
eyes usually closed
resistance to eye opening
intact pupillary response
can last several hours
injury possible
seconds-hours to reorientation
occasional incontinence
side to side head movements common
228
Q

define the different types of status epilepticus

A

impending status epilepticus/early status; <5 mins
status epilepticus; >5 mins
refractory status epilepticus; >30 mins
super refractory status epilepticus; >24hrs

229
Q

what investigations should be performed to diagnose status epilepticus?

A 
ABG
bloods
CTB
drug levels
ECG
EEG
230
Q

what are the causes of status epilepticus?

A

stroke (haemorrhagic)
low AED levels
alcohol withdrawal
drug intoxication; theophylline, imipenem, isoniazid, beta lactams, clozapine, bupropion
drug withdrawal; benzodiazepine, barbiturate, baclofen
anoxic brain injury
metabolic disturbances
infection; meningitis, encephalitis, brain abscess, sepsis
traumatic brain injury
brain neoplasm
febrile seizures
remote brain injury.congenital malformations
idiopathic

231
Q

what are the symptoms and signs of early status epilepticus?

A

compensation phase/sympathetic overdrive;
generalised convulsions
increased CO, BP, BG, blood lactate
increased cerebral blood flow, glucose and oxygen, brain tissue oxygenation, brain glucose

232
Q

what are the symptoms and signs of refractory/malignant status epilepticus?

A 
decompression/homeostatic failure;
reduced CO, BG, blood lactate, blood oxygen
cardiorespiratory collapse
electrolyte imbalances
rhabdomyolysis and delayed tubular necrosis
hyperthermia
multiple organ failure
increased brain damage
233
Q

what is the management of a post-epileptic event?

A

EEG monitoring essential if post-octal for a prolonged period
maintenance medication; consider higher dose
speak with neuro and ICU

234
Q

describe epilepsy in pregnancy

A

increased risk of obstetric complications; C-section, premature labour, bleeding
AEDs associated with neural tube defects, cleft palate. cardiac abnormalities, hypospadias (especially valproate, phenytoin, carbamazepine)
AED concentrations fluctuate during pregnancy; try to balance optimal seizure control with minimal foetal AED exposure
folate supplements recommended

235
Q

what investigations are required to diagnose a LMN lesion?

A 
CK; in all patients with neuromuscular weakness
neurophysiology
muscle biopsy
MRI spine; exclude other causes
muscle MRI
genetic testing
236
Q

what are the muscle biopsy features in inclusion body myositis?

A

endomysial inflammatory infiltrates
partial invasion of fibres
rimmed vascuoles
amyloid deposits on electron microscopy

237
Q

what functions are the extrapyramidal tracts responsible for?

A

posture

complex coordination of movement

238
Q

define UMN lesions

A

damage of upper motor neurone in the higher centre or above the level of the alpha motor neurone;
motor cortex
internal capsule
brain stem
spinal cord
contralateral weakness; above the decussation in the brainstem

239
Q

describe hemiplegia (UMN)

A 
contralateral weakness or paralysis
spasticity of the skeletal muscle due to increased supra spinal facilitation
exaggerated tendon jerk and clonus
positive babinskis sign
no atrophy
240
Q

define LMN lesions

A

damage of the lower motor neurons or any component of the reflex arc;
spinal cord
motor nerve axon
neuromuscular junction
muscle
sensory nerve
ipsilateral weakness, localised to muscles of the affected nerves

241
Q

what are the structural effects of LMN lesions?

A

nerve injury
retrograde degeneration
muscle atrophy
regeneration

242
Q

what are the functional effects of LMN lesions?

A 
all reflexes lost
very focal weakness
muscle wasting
fasciculations; appears a few days/weeks after denervation
weakness
reduced tone
243
Q

define fasciculations

A

synchronous visible contraction of the motor unit supplied by the injured axon
result from spontaneous generation of action potential in distal segment of the injured axon

244
Q

name examples of a generalised LMN process

A

generalised neuropathy; diabetic, GBS
myopathy; dermatomyositis, DMD
NMJ disorder; MG

245
Q

what is the aetiology of parkinsons disease?

A

sporadic/idiopathic
genetic; juvenile PD, young-onset PD, early onset <50yrs
drug induced; MPTP
post-infectious; encephalitis lethargica
chronic traumatic encephalopathy; boxing, rugby, football

246
Q

what are the features of Lewy body dementia?

A

fluctuating cognition
visual hallucinations
Parkinsonism

247
Q

what is the difference between LBD and PD?

A

LBD; Lewy bodies in cerebral cortex

PD; in substantis nigra

248
Q

describe MSA

A

MSA-P; Parkinsonism type
MSA-C; cerebellar type

alpha-synuclein

progresses more rapidly than PD
life expectancy 6-9 years from symptom onset

249
Q

describe PSP

A

accumulation of Tau protein

death usually within 7 years

250
Q

describe CBS

A

less common than MSA or PSP
pathology; Tau
onset usually around 63yrs
death within 8 years

251
Q

describe the classification of dystonia

A

area affected; focal or generalised
age of onset; juvenile or late
secondary to other degenerative disease

252
Q

describe motor tics

A

simple; blinking, pouting, facial grimacing

complex; kicking, jumping, hopping

253
Q

describe vocal tics

A

simple; grunting, sniffing, coughing

complex; echolalia, coprolalia

254
Q

what is the difference between spasticity and rigidity?

A

spasticity; velocity dependent, clasp knife, ground in UMN/pyramidal disease
rigidity; stiffness throughout the movement, lead pipe

255
Q

define akathisia

A

unpleasant sensation of restlessness

manifests as inability to sit still or remain motionless

256
Q

describe the causes, treatment and complications of bells palsy?

A

causes; HSV, VZV infection of the facial nerve
treatment; acyclovir, steroids
complications; persistent weakness, contracture, synkinesis

257
Q

describe synkinesis

A

voluntary muscle movement causes the simultaneous involuntary contraction of other muscles
crocodile tears

258
Q

describe the course of the hypoglossal nerve

A

arises from the hypoglossal nucleus in the medulla oblongata
passes laterally over the posterior cranial fossa
exits the cranium via the hypoglossal canal
passes inferiorly to the angle of the mandible
moves anteriorly to enter the tongue

259
Q

what are the causes of hypoglossal nerve palsy?

A

head and neck malignancy
penetrating trauma injuries
internal carotid artery dissection

260
Q

what are the clinical features of trigeminal neuralgia?

A

sudden, short lasting, shooting/shock pain
unilateral
worse when eating and drinking
can’t bear to touch it

treatment; carbamazepine

261
Q

what are the locations and features of cranial nerve damage?

A

CN nucleus within the brainstem
nerve axons form nucleus still within the brainstem
outside the brainstem

weakness
ataxia
sensory loss

262
Q

what are the symptoms of anterograde amnesia?

A 
forgetting recent personal/family events
losing things in the house
repeating questions, conversations
problems following TV or noels
reliance on lists
263
Q

what are the symptoms of retrograde amnesia?

A

past events; jobs, homes, illnesses, major news items

getting lost in familiar surrounds

264
Q

what are the functions of the temporal lobes?

A

memory;
episodic
semantic

265
Q

what are the functions of the perisylvian areas?

A

langauge

266
Q

what are the functions of the frontal lobes?

A

behavioural change

executive function

267
Q

what are the functions and pathologies of the parietal lobes?

A

praxis
visuoconstructive
tactile agnosia
gerstmann’s syndrome

268
Q

what are the functions and pathologies of the occipital lobes?

A

visual agnosia

ballint’s syndrome

269
Q

what are the functions of the orbitofrontal lobes?

A 
personality and behaviour;
disinhibition
eating behaviours
lack of empathy
personal neglect
poor judgement

motivation;
apathy
passivity

270
Q

describe gerstmann’s syndrome

A 
damage to the left angular gyrus
acalculia
agraphia
left/right disorientation
finger agnosia
271
Q

what is the definition and causes of apraxia?

A

inability to perform learned skilled movements despite normal motor, sensory function, coordination, comprehension and attention

dominant parietal, inferior frontal lesions or anterior corpus callosum

272
Q

what is the definition and causes of unilateral neglect?

A

failure to report, respond or orient to stimuli presented contralateral to a brain lesion not due to elementary sensory or motor disorder

right parietal lesions
also thalamus, basal ganglia, cingulate
usually affects LHS

273
Q

define visual agnosia

A

failure of recognition despite normal visual percepts

274
Q

describe associative visual agnosia

A

preserved ability to perceive detail and copy accurately but unable to recognise what they have drawn
left; words
right; faces
bilateral; objects

275
Q

describe Alzheimer’s disease

A

> 30yrs onset, usually >60yrs
on average 8 years duration
medial temporal lobes; amnesia
temporo-parietal lobes; visuospatial deficits, language
treatment; cholinesterase inhibitors (donepezil)

276
Q

describe frontotemporal dementia

A 
usually 45-65yrs onset
2-20yrs duration
frontal lobes; behavioural onset
perisylvian areas; progressive aphasia
anterior temporal lobes; semantic memory
277
Q

describe semantic dementia

A

a subtype of frontotemporal dementia
language problems
impaired word comprehension
naming errors

278
Q

describe Lewy body dementia

A 
usually >40yrs onset, mostly >65yrs
1-12yrs duration
medial temporal lobes and temporoparietal; similar to AD, more visuospatial difficulty
substantia nigra; Parkinsonism
visual hallucinations, fluctuations
neuroleptic sensitivity
279
Q

describe vascular dementia

A 
usually >40yrs onset, mostly >65yrs
variable, up to 12 yrs duration
features determined by infarct location
stepwise decline
pseudo bulbar palsy
pyramidal signs
extensor plantars

Clinical Practice (14 decks)

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