neuro Flashcards
1
Q
nerve malfunction: demyelination
A
- schwann cell damage leads to myelin sheath disruption
- results in marked slowing of conduction
- seen for example- in guillain-barre syndrome
2
Q
nerve malfunction: axonal degeneration
A
- axon damage causes the nerve fibre to die back from periphery
- conduction velocity initially remains mortal because axonal continuity is maintained in surviving fibres
- typically occurs in toxic neuropathies
3
Q
nerve malfunction: compression
A
- focal demyelination at point of compression causes disruption of conduction
- typically occurs in entrapment neuropathies
4
Q
nerve malfunction: infarction
A
-micro infarction of vasa nervorum occurs in diabetes and arteritis
5
Q
nerve malfunction: infiltration
A
infiltration occurs by inflammatory cells in leprosy and granulomas such as sarcoid and neoplastic cells
6
Q
nerve malfunction: wallerian degeneration
A
process that results when a nerve fibre is cut and distal part of the axon that is separated from neurone’s cell body degenerates
7
Q
neuropathy
A
pathological process affecting a peripheral nerve or nerves
8
Q
mononeuritis multiplex
A
means that several individual nerves are affected
9
Q
mononeuropathies
A
process affects a single nerve
10
Q
carpal tunnel syndrome
A
most common mononeuropathy and entrapment neuropathy
11
Q
carpal tunnel syndrome: pathology
A
results from pressure and compression on the median nerve as it passes through carpal tunnel in the wrist
12
Q
carpal tunnel syndrome: epidemiology
A
more common in females
females have narrower wrists but same sized tendons
usually in those >30 y/o
13
Q
carpal tunnel syndrome: causes
A
usually idiopathic
14
Q
carpal tunnel syndrome: associations
A
hypothyroidism diabetes mellitus pregnancy (3rd trimester) amyloidosis obesity rheumatoid arthritis acromegaly
15
Q
carpal tunnel syndrome: risk factors
A
diabetes
16
Q
carpal tunnel syndrome: presentation
A
- aching pain in hand and arm, especially at night
- paraesthesiae (tingling or prickling) in thumb, index, middle + 1/2 ring fingers, and palm
17
Q
carpal tunnel syndrome: differentials
A
peripheral neuropathy
motor neurone disease
MS
18
Q
carpal tunnel syndrome: electromyography
A
shows slowing of conduction velocity in median sensory nerves across carpal tunnel
helps confirm lesion site and severity
19
Q
carpal tunnel syndrome: phalen’s test
A
patient can only maximally flex wrist for 1 minute
20
Q
carpal tunnel syndrome: tinel’s test
A
tapping on the nerve at the wrist induces tingling
21
Q
carpal tunnel syndrome: treatment
A
wrist splint at night
local steroid injection
decompression surgery
22
Q
mononeuropathies: ulnar nerve (C7-T1)
A
vulnerable to elbow trauma
compression mostly occurs at epicondylar groove at point where nerve passes between 2 heads of flexor carpi ulnaris
23
Q
mononeuropathies: ulnar nerve (C7-T1) signs
A
weakness/wasting of:
- medial wrist flexors
- interossei
- medial 2 lumbricals
24
Q
mononeuropathies: ulnar nerve (C7-T1) treatment
A
rest and avoiding pressure on the nerve
night time soft elbow splinting
25
mononeuropathies: radial nerve (C5-T1)
nerve opens the fist
| it may be damaged by compression against the humerus
26
mononeuropathies: radial nerve (C5-T1) signs
```
test for wrist and finger drop
muscles involved= BEST
Brachioradialis
Extensor
Supinator
Tricep
```
27
mononeuropathies: phrenic nerve (C3-5)
consider phrenic palsy if orthopnoea (SOB while lying flat) with raised hemidiaphragm on CXR
28
mononeuropathies: phrenic nerve (C3-5) causes
```
lung cancer
myeloma
thymoma
cervical spondylosis
phrenic nucleus lesion
thoracic surgery
HIV
muscular dystrophy
```
29
mononeuropathies: sciatic nerve (L4-S3)
damaged by pelvic tumours or fractures to pelvis or femur
| lesions affect the hamstrings and all muscles below knee- foot drop
30
mononeuropathies: common peroneal nerve (L4-S1)
originates from sciatic nerve above the knee
| often damaged as it winds around the fibular head due to trauma or sitting cross-legged
31
mononeuropathies: common peroneal nerve (L4-S1) signs
foot drop
weak ankle dorsiflexion
sensory loss over dorsum of foot
32
polyneuropathies
diffuse, symmetrical disease usually commencing peripheral
| can be motor, sensory, sensorimotor and autonomic
33
polyneuropathies: classification
acute or chronic
sensory/motor/autonomic/mixed
demyelination, axonal degeneration or both
34
polyneuropathies: causes
metabolic- diabetes, renal failure, hypothyroidism
malignancy- paraneoplastic syndromes
inflammatory- guillain-barre syndrome, sarcoidosis
infections- leprosy, HIV, syphilis
35
polyneuropathies: sensory neuropathy presentation
numbness
affects extremities first
difficulty handling small objects
signs of trauma
36
polyneuropathies: motor neuropathy presentation
often rapidly progressive
weak or clumsy hands
difficulty walking and breathing
37
cranial nerve 3 lesions
oculomotor palsy
ptosis- dropping eyelids
fixed dilated pupil
eye down and out
38
cranial nerve 3 lesions: causes
raised intracranial pressure
diabetes
hypertension
giant cell arteritis
39
cranial nerve 6 lesions
abducens palsy
| innervate lateral rectus muscle thus eyes will be adducted
40
cranial nerve 6 lesions: causes
MS
wernicke's encephalopathy
pontine stroke
41
cranial nerves 3, 4 & 6 lesions
non functioning eye
42
cranial nerves 3, 4 & 6 lesions: causes
stroke
tumours
wernicke's encephalopathy
43
cranial nerve 5 lesions
trigeminal palsy
jaw deviates to side of lesion
loss of corneal reflex
caused by trigeminal neuralgia, herpes zoster
44
cranial nerve 7 lesions
facial palsy
| facial droop and weakness
45
cranial nerve 7 lesions: causes
bells palsy= most common lesion
fractures of petrous bones
middle ear infections
46
cranial nerve 8 lesions
vestibulocochlear palsy
hearing impairment
vertigo and lack of balance
47
cranial nerve 8 lesions: causes
skull fracture
toxic drug effects
ear infections
48
cranial nerves 9 & 10 lesions
glossopharyngeal and vagus palsy
| gag reflex issues, swallowing issues, vocal issues
49
autonomic neuropathy
sympathetic and parasymp neuropathies may be isolated or part of a generalised sensorimotor peripheral neuropathy
50
autonomic neuropathy: causes
diabetes
guillain-barre
HIV
SLE
51
autonomic neuropathy: sympathetic presentation
postural hypotension- faints on standing, eating or hot bath
ejaculatory failure
reduced sweating
52
autonomic neuropathy: parasymp presentation
erectile dysfunction
constipation
nocturnal diarrhoea
urine retention
53
polyneuropathy: diagnosis
FBC, ESR, glucose, U&E, LFT, TSH, B12
CXR
urinalysis
lumbar puncture
54
polyneuropathy: treatment
treat the cause
foot care and shoe choice
splinting of joints
55
Nerve root lesion @ L2: Pain, weakness, reflex affected
pain- across upper thigh
weakness- hip flexion and adduction
reflex- N/A
56
Nerve root lesion @ L3: Pain, weakness, reflex affected
pain- across lower thigh
weakness- hip adduction, knee extension
reflex- knee jerk
57
Nerve root lesion @ L4: Pain, weakness, reflex affected
pain- across knee to medial malleolus
weakness- knee extension, foot inversion, dorisflexion
reflex- knee jerk
58
Nerve root lesion @ L5: Pain, weakness, reflex affected
pain- lateral shin to dorsum of foot and great toe
weakness- hip extension and abduction, knee flexion
reflex- great toe jerk
59
Nerve root lesion @ S1: Pain, weakness, reflex affected
pain- posterior calf to lateral foot and little toe
weakness- knee flexion, foot and toe plantar flexion
reflex- ankle jerk
60
focal scalp lesions
contusions
| lacerations
61
focal skull lesions: fracture
implies considerable force
high risk of haematoma, infection and aerocele
pointed objects cause localised fractures
flat surfaces cause linear fractures
62
focal meninges lesions: extradural haematoma
10% of severe injuries, 15% of fatal ones
associated with skull fracture
occurs slowly over hours
63
focal meninges lesions: extradural haematoma causing death
brain displacement
raised intracranial pressure
herniation
infection
64
focal meninges lesions: subdural haematoma
usually due to tears in bridging veins- cross subdural space from superior surface of brain to midsagittal sinus
occurs slowly
65
focal meninges lesions: traumatic subarachnoid haematoma causes
contusions
base of skull fracture
vertebral artery dissection
intraventricular haemorrhage
66
focal brain lesions: contusions
superficial bruises on the brain
coup or contre coup
haemorrhagic then brown and soft for days-weeks and then indented or cavitated after months
67
focal brain lesions: lacerations
when contusion is sufficiently severe to teat the pia mater
68
focal brain lesions: haemorrhage
cerebral or cerebellar haemorrhage
superficial- due to severe contusion
deep- related to diffuse axonal injury
69
focal brain lesions: infection
predominantly due to skull fracture
70
diffuse brain lesions: diffuse axonal injury
clinicopathological syndrome of widespread axonal damage
| can be caused by variety of processes
71
diffuse brain lesions: diffuse vascular injury
usually a result of near immediate death
| multiple petechial haemorrhages throughout brain
72
diffuse brain lesions: hypoxia-ischaemia
often causes infarction and damage
| likely in pts. with evident hypoxia, hypotension and/or raised intracranial pressure
73
diffuse brain lesions: swelling
occurs in 75% of pts.
| causes raised intracranial pressure
74
diffuse brain lesions: congestive brain swelling
vasodilation and increased cerebral blood volume
75
diffuse brain lesions: vasogenic oedema swelling
extravasation of oedema fluid from damaged blood vessels
76
diffuse brain lesions: cytotoxic oedema swelling
increased water content of neurons and glia
77
coup vs. contre coup injuries
coup= occurs under site of impact from an object
| contre coupe= occurs on side opposite area that was hit
78
traumatic axonal injury
focal or widespread
usually involves acceleration and deceleration of the head
mild= recovery of consciousness, variable severity of deficit
severe= unconscious from impact, can remain so or severe disability
79
meningitis
inflammation of the meninges
| can be infective or non-infective (drugs, autoimmune)
80
encephalitis
inflammation of the brain
| usually viral
81
encephalopathy
reduced level of consciousness/diffuse disease of brain substance
usually non-infective with multiple aetiologies
82
polyradiculopathy
inflammation of nerve roots e.g. cauda equina
83
myelitis
inflammation of spinal cord
84
meningitis: epidemiology
occurs in people of all age groups but more common in infants/elderly
meningococcal disease is notifiable to public health england
85
meningitis: aetiology; adults and children
neisseria meningitides- gram negative diplococci
| streptococcus pneumoniae/pneumococcus
86
meningitis: aetiology; pregnancy/older adults
listeria monocytogenes- found in cheese so why theyre told to avoid
87
meningitis: aetiology; neonates
escheria coli
| group b haemolytic streptococcus
88
meningitis: aetiology; immunocompromised
cytomegalovirus
TB
HIV
herpes simplex virus
89
meningitis: risk factors
```
intrathecal drug administration
immunocompromised
elderly
pregnant
crowding- uni students
diabetes
IV drug abuse
```
90
bacterial meningitis: pathophysiology
typically sudden
N. meningitides is transmitted by droplet spread
pia-arachnoid is congested with polymorphs
layer of pus forms which can form adhesions causing cranial nerve palsied and hydrocephalus
91
bacterial meningitis: meningococcal septicaemia pathophsyiology
bacteria invades into blood
| presence of endotoxin in bacteria causes inflammatory cascade
92
chronic meningitis: pathophysiology
e.g. TB
| brain is covered in a viscous grey-green exudate with numerous meningeal tubercles
93
viral meningitis: pathophysiology
predominantly lymphocytic inflammatory CSF reaction w/o pus formation
little of no cerebral oedema unless encephalitis develops
94
bacterial meningitis: presentation
triad= headache, neck stiffness and fever
sudden onset
intense malaise, rigor, photophobia and vomiting
irritable
seizures and CNS signs
papilloedema
95
bacterial meningitis: papilloedema
swelling of optic disc on fundoscopy
usually bilateral
can occur over hours to weeks
caused by raised intracranial pressure
96
viral meningitis: presentation
triad
benign, self limiting condition lasting 4-10 days
headache may follow for some months
97
chronic meningitis: presentation
mycobacterium tuberculosis
long history and vague symptoms of headache, anorexia and vomiting
signs of meningeal triad are often absent or late
98
meningitis: differentials
aseptic meningitis- due to tumour
sub-arachnoid haemorrhage
encephalitis
99
meningitis: investigations
blood culture before lumbar puncture
FBC, U&E, CRP and serum glucose
throat swab
100
meningitis: investigations; lumbar puncture
@L4
send for microscopy and sensitivity
can give headache, paresthesia, CSF leak and damage to spinal cord
101
meningitis: lumbar puncture results; TB
lymphocytes
raised protein
low/normal glucose
102
meningitis: lumbar puncture results; Virus
lymphocytes
normal protein
normal glucose
103
meningitis: lumbar puncture results; bacteria
neutrophil polymorphs
raised protein
low glucose
104
meningitis: investigations; CT head
```
exclude lesions such as tumours
to do CT before lumbar puncture:
- >60y/o
-immunocompromised
-history of CNS disease
-new onset of seizures
-GCS <14
```
105
meningitis: investigations; non- blanching petechial or purpuric rash
purpuric rash +signs of sepsis= meningococcal septicaemia
immediate IV benzylpenicillin or IV cefotaxime
don't do lumbar puncture, instead of blood cultures
106
bacterial meningitis: treatment
if suspect bacterial- start antibiotics before tests come back
IV cefotaxime
if immunocompromised then add IV amoxicillin to cover listeria
consider steroids, dexamthasone to reduce oedema
107
encephalitis: epidemiology
infections are most frequent in children and elderly- mainly viral cause
more common in immunocompromised
108
encephalitis: viral aetiology
```
herpes simplex virus 1 and 2
varicella zoster
epstein barr
HIV
mumps and measles
```
109
encephalitis: non viral aetiology
bacterial meningitis
TB
malaria
110
encephalitis: risk factors
extremes of age
| immunocompromised
111
encephalitis: pathophysiology
disease which mostly affects the frontal and temporal lobes resulting in decreased consciousness, confusion and focal signs
112
encephalitis: general presentation
whole brain affected- problems with consciousness
can be abrupt in onset
triad= fever, headache and altered mental status
113
encephalitis: early presentation
begins with features of viral infection
| fever, headache, myalgia, fatigue and nausea
114
encephalitis: progressive presentation
```
personality and behavioural changes
decreased consciousness, confusion and drowsiness
hemiparesis, dysphasia
seizures
coma
```
115
encephalitis: differentials
meningitis
stroke
brain tumour
116
encephalitis: MRI
shows area of inflammation and swelling, generally in temporal lobes in HSV
117
encephalitis: electroencephalography
shows periodic sharp and slow wave complexes
118
encephalitis: lumbar puncture
CSF shows elevated lymphocyte count
| viral detection by CSF, PCR is highly sensitive for herpes simplex and varicella zoster
119
encephalitis: treatment
if viral then immediate treatment with anti-viral- IV aciclovir
anti seizure medication- primidone
120
herpes zoster
shingles
virus remains latent in sensory ganglia
caused by reactivation of varicella zoster (chicken pox) usually within the dorsal root ganglia
121
herpes zoster: epidemiology
90% of children exposed to chicken pox before age of 16
| can affect all ages but seen in elderly
122
herpes zoster: aetiology
varicella zoster virus
123
herpes zoster: risk factors
increasing age
immunocompromised
HIV
bone marrow transplants
124
herpes zoster: pathophysiology
viral infection affecting peripheral nerves
when latent virus is reactivated in dorsal root ganglia it travels down the affected nerve via sensory root- dermatomal distribution
result in perineural and intramural inflammation
125
herpes zoster: presentation
pain and paresthesia in dermatomal distribution
malaise, myalgia, headache and fever
rash
126
herpes zoster: rash presentation
consists of papules and vesicles restricted to same dermatome
neuritic pain
crust formation and drying occurs over next week w/ resolution in 2-3 weeks
infectious until lesions are dried
127
herpes zoster: differentials
before rash:
pain in chest or abdo pain- cholecystitis or renal stones
cluster headaches or migraine
128
herpes zoster: diagnosis
rash is virtually diagnostic
129
herpes zoster: treatment
oral antiviral therapy w/i 72 hours of rash onset (aciclovir x5 daily)
topical antibiotic for secondary infection of rash
analgesia for pain
130
herpes zoster: post herpetic neuralgia
pain lasting more than 4 months after shingles
occurs in 10%
burning, intractable pain
responds poorly to analgesics
131
herpes zoster: post herpetic neuralgia treatment
tricyclic antidepressant- amitriptyline
anti-epileptic- gabapentin
anti-convulsant- carbamezapine
132
tetanus: pathology
inoculation through skin with clostridium tetani spores- found in soil
bacteria produce toxins such as tetanolysin- tissue destruction
tetanospasmin- clinical tetanus
133
tetanus: pathogenesis
tetanospasmin can travel retrogradely along axons
| interferes with neurotransmitter release, increased neuron firing, unopposed muscle contraction and spams
134
tetanus: generalised presentation
risus sardonicus- abnormal, sustained spasm of facial muscles that appears to produce grinning
opisthotonos- spasm of muscles causing backward arching of the head, neck and spine
135
tetanus: localised presentation
e.g.
| injury to R hand, 2 days later unopposed flexion of fingers and spasm in forearm
136
tetanus: prevention
better than cure
| vaccinate
137
tetanus: symptomatic treatment
supportive- muscle relaxants, paracetamol
immunoglobulin to mop up toxin
metronidazole to clear residual bacteria
138
rabies: pathology
caused by rabies lyssavirus, formerly rabies virus
kills 35-50 thousand/yr
inoculation through skin with saliva of rabid animals
travels retrogradely along nerves
139
rabies: incubation
depends on size and site of inoculation
| min 2 weeks, max 2 years
140
rabies: presentation
paresthesia at bite site
reaches CNS- furious or paralytic presentation
once symptomatic, invariably fatal, >99.9%
141
rabies: treatment
managed with sedatives
| prophylaxis- PrEP (vaccination) or PEP
142
dementia
a syndrome caused by a number of brain disorders which cause memory loss, difficulties with thinking, problem solving or language as well as difficulties with activities of daily living
143
dementia: epidemiology
rare under 55 y/o
prevalence rises with age
AD more common in females than males
144
alzheimer's dementia: aetiology
50%
most common cause
degeneration of cerebral cortex
accumulation of beta-amyloid peptide, a degradation product of amyloid precursor protein- results in progressive neuronal damage
145
vascular dementia: aetiology
25%
brain damage due to cerebrovascular disease, either major stroke, multiple smaller unrecognised strokes
presents with signs of vascular pathology
146
lewy-body dementia: aetiology
15%
deposition of abnormal protein with neurones in brain stem and neocortex
associated with parkinson's
147
fronto-temporal dementia: aetiology
specific degeneration/atrophy of frontal and temporal lobes of the brain
behavioural and personality change, early preservation of episodic memory and spatial orientation
148
dementia: risk factors
```
family history
age
down's syndrome
alcohol use, obesity, high BP
atherosclerosis
depression
```
149
alzheimer's dementia: presentation
insidious onset with steady progression over years
short term memory loss is usually the most prominent early symptoms
slow disintegration of personality and intellect
decline in language skills
150
vascular dementia: presentation
stepwise deterioration with declines followed by short periods of stability
history of TIAs and/or strokes
evidence of arthropathy
151
dementia: presentation of Lewy bodies
```
fluctuating cognition with pronounced variation in attention and alertness
persistent memory loss
impairment in attention
depression and sleep disorders
visual hallucinations
```
152
dementia: differentials
substance abuse
hypothyroidism
huntington's
153
dementia: investigations
mini mental state examination commonly used to screen for cognitive function
MRI to see atrophy
154
dementia: prevention
no specific therapy
healthy behaviour- smoking cessation, good diet, low alcohol
>6 leisure activities lowers risk
155
dementia: supportive care
socially active- sees friends and families
cognitively active
specialist memory service
156
multiple sclerosis
chronic autoimmune, T-cell mediated inflammatory disorder of the CNS in which there are multiple plaques of demyelination w/i brain and spinal cord
157
multiple sclerosis: epidemiology
begins early adulthood, typically 20-40 y/o
more common in females
more common in white populations
158
multiple sclerosis: aetiology
not understood
| combination of genetics and environment
159
multiple sclerosis: pathophysiology
autoimmune mediated demyelination at multiple CNA sites- targeting oligodendrocytes
thought to be T cell mediated- activate B cells to produce auto-antibodies against myelin
myelin sheath regenerates but it is less efficient and when exposed to high heat conduction decreases drastically
160
types of multiple sclerosis: relapsing & remitting
80%- most common
symptoms occur in attacks with onset over days and typically recovery- partial or complete
periods of good health or remission are followed by sudden symptoms or relapses
161
types of multiple sclerosis: secondary progressive
follows from relapsing and remitting (75% of RR get secondary)
late stage that consists of gradually worsening symptoms with fewer remissions
162
types of multiple sclerosis: primary progressive
gradually worsening disability w/o relapses or remissions
| typically presents later and is associated with fewer inflammatory changes on MRI
163
multiple sclerosis: presentation
```
usually initially monosymptomatic
symptoms may worsen with heat
numbness and tingling in limbs
leg weakness
trigeminal neuralgia
constipation
intension tremor
amnesia
sexual dysfunction
```
164
multiple sclerosis: unilateral optic neuritis presentation
pain in one eye on eye movement
| reduced central vision
165
multiple sclerosis: brainstem demyelination presentation
diplopia, vertigo, facial numbness, dysarthria or dysphagia
| clumsy/useless hand or limb due to loss of proprioception
166
multiple sclerosis: differentials
hereditary spastic paraplegia
cerebral variant of SLE
sarcoidosis
HIV
167
multiple sclerosis: investigations
requires 2+ attacks affecting different parts of CNS- 2 lesions disseminated in time and space
exclude differentials with inflammatory markers, auto-antibodies, calcium and LFTs
168
multiple sclerosis: MRI brain and spinal cord
diagnostic
95% have periventricular lesions
over 90% show discrete white matter abnormalities
169
multiple sclerosis: lumbar puncture
CSF examination shows oligoclonal IgG bands in over 90% of cases- not specific to MS
170
multiple sclerosis: electrophysiology investigation
visual evoked potential studies
| delayed nerve conduction suggests demyelination
171
multiple sclerosis: acute relapse treatment
IV methylprednisolone
<3 days can shorten relapse
use steroid sparingly and aim to use less than twice a year
172
multiple sclerosis: treatment for frequent relapse
SC interferon 1B or 1A are anti-inflammatory cytokine and reduce relapses by 30% in active remitting MS and reduce lesion accumulation
dimethyl fumarate
monoclonal antibodies
173
multiple sclerosis: monoclonal antibodies
disease modifying agents
IV alemtuzumab- targets T cells
IV natalizumab- against VLA-4 receptors that allow autoimmune cells to cross BBB
174
multiple sclerosis: symptomatic treatment
urinary urgency/frequency- self catheterisation
incontinence- anti cholinergic alpha blocker (doxazosin)
spasticity- physio, baclofen, botox injection
175
epilepsy: definition
recurrent tendency to spontaneous, intermittent, abnormal electrical activity in part of the brain
manifests as seizures
chronic disorder- at least 2 seizures to be diagnosed
176
epilepsy seizure definition
paroxysmal/unprovoked event in which changes in behaviour, sensation or cognitive are caused by excessive, hypersynchronous neuronal discharges in the brain
177
epilepsy: epidemiology
common
highest at extremes of age- <20 y/o or >60 y/o
can go into remission
178
epilepsy: aetiology
```
2/3rds idiopathic
often familial
stroke
space occupying lesion- tumour
alcohol withdrawal
cortical scarring
```
179
epilepsy: risk factors
```
family history
premature babies
abnormal blood vessels in brain
alzheimers
use of drugs- cocaine
stroke/tumour/infection
```
180
epilepsy: elements of a seizure
prodome
aura
post-ictally
181
epilepsy pathophysiology: prodome
lasting hours or days
may rarely precede the seizure
not part of seizure, results in change of mood/behaviour
182
epilepsy pathophysiology: aura
part of seizure
patient is aware and may precede its other manifestations
strange feeling in gut, deja vu, strange smells/lights
implies focal seizure often but not necessarily temporal lobe
183
epilepsy pathophysiology: post-ictally
```
after seizure
headache
confusion
myalgia
temporary weakness if its in motor cortex
```
184
epilepsy pathophysiology: primary generalised
simultaneous onset of electrical discharge throughout whole cortex
no localising features referable to one hemisphere
bilateral, symmetrical manifestations
loss of consciousness
185
epilepsy pathophysiology: partial/focal seizures
features referable to part of one hemisphere/lobe
| often seen with underlying structural disease
186
epilepsy presentations: generalised tonic-clonic seizure
often no aura
loss of consciousness
tonic= rigid, stiff limbs, falls to floor
clonic=bilateral, rhythmic muscle jerking, seconds to minutes
eyes open and tongue often bitten
incontinence
187
epilepsy presentations: typical absence seizure
usually disorder of childhood
ceases activity, stares and pales for a few seconds
often don't realise anything happened
tend to develop tonic-clonic in later life
188
epilepsy presentations: myoclonic seizure
sudden isolated jerk, face or trunk
patient may be thrown suddenly to ground
violently disobedient limb
189
epilepsy presentations: tonic seizure
sudden sustained increased tone with cries/grunts
| not followed by jerking
190
epilepsy presentations: atonic seizure
sudden loss of muscle tone and cessation of movement
191
epilepsy presentations: simple partial seizure
not affecting consciousness or memory
awareness if unimpaired in motor, sensory, autonomic or psychic focal seizures
no post-ictal
192
epilepsy presentations: complex partial seizure
affect awareness or memory before, during or immediately after seizure
commonly arise from temporal lobe- speech, memory and emotion
post-ictal confusion
193
epilepsy presentations: partial seizure w/ secondary generalisation
in 2/3rds of patients with partial seizures the electrical disturbance starts focally then spreads
causes a secondary generalised seizure- usually convulsive
194
epilepsy presentations: temporal lobe involvement
```
aura 80%
deja-vu
auditory hallucinations
funny smells
anxiety
out of body experience
```
195
epilepsy presentations: frontal lobe involvement
motor features such as posturing or movement of leg
Jacksonian march= seizure marches up or down motor homunculus starting in face or thumb
post-ictal Todd's palsy= paralysis of limbs involved
196
epilepsy presentations: occipital lobe involvement
visual phenomena
197
epilepsy presentations: epilepsy rather than syncope
```
tongue biting
head turning
muscle pain
loss of consciousness
cyanosis
post-ictally
```
198
epilepsy presentations: syncope rather than epilepsy
syncope= loss of consciousness due to hypoperfusion to the brain
199
epilepsy presentations: non-epileptic seizure vs. epileptic
non-epileptic= situational, longer, close mouth/eyes, do not result from sleep, no incontinence
200
epilepsy differential diagnosis
```
postural syncope
cardiac arrhythmia
TIA
migraine
panic attack
non-epileptic seizure
```
201
epilepsy investigations
EEG
MRI/CT head
blood tests
genetic testing
202
epilepsy investigations: electroencephalogram
not diagnostic
performed to support diagnosis of epilepsy when history suggests
may help determine seizure type
203
epilepsy investigations: MRI
imaging hippocampus studies epilepsy
204
epilepsy investigations: CT head
used in emergency to look for space occupying lesion
| identify or exclude structural abnormalities that could cause symptoms
205
epilepsy investigations: blood tests
done to rule out metabolic cause
discover comorbidities
FBC, electrolytes, Ca2+, renal function
206
epilepsy treatment
generally drugs are not advised after just one fit unless the risk of recurrence is high
drug resistant to drug treatment in 1/3rd of patients
207
epilepsy treatment: emergency measures
ensure they harm themselves as little as possible
check glucose
prolonged seizure (>3min) or repeated are treated with rectal/IV diazepam or loraezepam x2
IV phenytoin loading
208
epilepsy treatment: for generalised tonic-clonic seizures
oral sodium volproate- S/E =weight gain and hair loss
oral lamotrigine- S/E= maculopapular rash, blurred vision
oral carbamazepine- S/E= diplopia, rashes, impaired balance
209
epilepsy treatment: for absence seizure
oral sodium valproate
oral lamotrigine
oral ethosuximide
210
epilepsy treatment: for partial/focal seizure
carbamazepine
sodium valproate
lamotrigine
211
epilepsy treatment: neurosurgical
if drugs don't work
| if a single defined cause if identified such as hippocampal sclerosis or tumour
212
epilepsy treatment: advice to patients
must inform DVLA and cannot drive until they have been free of daytime seizures for at least one year
213
epilepticus
repeated seizures with brief periods of recovery can lead to epilepticus
medical emergency
risk of death if generalised tonic-clonic
214
epilepticus: causes
abruptly stopping anti-epileptic treatment
alcohol abuse
poor compliance to therapy
215
sudden unexpected death epilepsy
more common in uncontrolled epilepsy
| can be related to nocturnal seizure-associated apnoea and asystole
216
TIA definition
transient ischaemic attack= a brief episode of neurological dysfunction due to temporary focal cerebral ischaemia w/o infarction
217
TIA epidemiology:
15% of first strokes are preceded by TIA
| more common in males
218
TIA aetiology
```
small vessel occlusion
atherothromboembolism from carotid
cardioembolism from microemboli
hyperviscosity
hypoperfusion
```
219
TIA aetiology: cardioembolism
microemboli come from:
mural thrombus post MI or AF
valve disease
prosthetic valve
220
TIA aetiology: hyperviscosity
polycythaemia
sickle cell anaemia
extremely raised white cell count
myeloma
221
TIA aetiology: hypoperfusion
consider in younger people
cardiac dysrhythmia
postural hypotension
222
TIA risk factors
```
increased age
hypertension
smoking
diabetes
heart disease
past TIA
excess alcohol
clotting disorder
combined oral contraceptive
```
223
TIA pathophysiology
most common cause is cerebral ischaemia- lack of oxygen and nutrients to brain causes cerebral dysfunction
usually short lived so symptoms last 5-15 mins and resolves itself
224
TIA presentation: carotid artery
supplies frontal and medial part of cerebrum
occlusion may cause weak, contralateral symptoms of limbs
hemiparesis (weakness on entire side of body)
dysphasia
amaurosis fugax
225
TIA presentation: amaurosis fugax
sudden transient loss of vision in one eye
| occurs due to reduction in retinal, ophthalmic or ciliary blood flow leading to temporary retinal hypoxia
226
TIA presentation: vertebrobasilar artery
```
diplopia- double vision
vertigo
vomiting
ataxia- no control over body
hemisensory loss
hemianopia vision loss
```
227
stroke definition
cerebrovascular accidents
| syndrome of rapid onset of neurological deficit caused by focal, cerebral, spinal or retinal infarction
228
stroke epidemiology
```
3rd most common cause of death in high income countries
11% of all deaths in UK
leading cause of adult disability
incidence increases with age
more common in males
```
229
stroke aetiology: ischaemic
```
80%
small vessel occlusion/thrombosis
cardiac emboli from AF or infective endocarditis
large artery stenosis
hypoperfusion
vasculitis
hyperviscosity
```
230
stroke aetiology: CNS bleeds
```
17%
trauma
aneurysm rupture
anticoagulation
thrombolysis
artery dissection
subarachnoid haemorrhage
```
231
stroke aetiology: young people
```
vasculitis
thrombophilia
subarachnoid haemorrhage
carotid artery dissection
venous sinus thrombosis
```
232
stroke aetiology: elderly
```
thrombosis in situ
atherothromboembolism
heart emboli
CNS bleed
sudden drop in BP
```
233
stroke risk factors
```
male
black or asian
hypertension
past TIA
smoking
diabetes
increasing age
heart disease
alcohol
AF
hypercholesterolaemia
combined contraceptive
```
234
stroke pathophysiology: ischaemic
arterial disease and atherosclerosis is main pathological process
235
stroke pathophysiology: cardio-embolic stroke
AF
cardiac valve disease
infective vegetations due to endocarditis
fat emboli
236
stroke pathophysiology: venous sinus thrombosis
very rare
thrombosis in intracranial venous sinuses
cortical infarction, seizures and raised intracranial pressure result
237
stroke pathophysiology: haemorrhagic
hypertension resulting in micro aneurysm rupture
cerebral amyloid angiopathy
carotid/vertebral artery dissection
238
stroke presentations: anterior cerebral artery
leg weakness
sensory disturbance in legs
gait apraxia
drowsiness
239
stroke presentations: middle cerebral artery
contralateral arm and leg weakness
contralateral sensory loss
hemianopia
aphasia- cant understand or produce speech
dysphasia- deficiency in speech generation
facial droop
240
stroke presentations: posterior cerebral artery
```
contralateral homonymous hemianopia
cortical blindness
visual agnosia but can see
prosopagnosia- cant see faces
colour naming problems
```
241
stroke presentations: vertebrobasilar artery
more catastrophic due to wide region supplied
locked in is more likely
motor deficits- hemiparesis or tetraparesis
facial paralysis
vertigo
visual disturbance
altered consciousness
242
stroke presentations: lacunar
small subcortical strokes
unilateral weakness of face and arm, arm and leg or all three
pure sensory loss
243
stroke presentations: haemorrhage or ischaemic
no reliable way to distinguish from presentation
haemorrhage is more associated with severe headache
if on anticoagulants- assume haemorrhage
244
stroke differentials
exclude hypoglycaemia
migraine
intracranial lesion
syncope
245
stroke investigations: urgent CT head
before treatment
rules out haemorrhage before starting thrombolysis
infarct is seen as low density lesion
246
stroke investigations: pulse, BP, ECG
look for AF
| be careful treating high BP as fall in 20% can compromise cerebral perfusion
247
stroke investigations: bloods
look for thrombocytopenia and polycythaemia in FBC
| rule out hypoglycaemia
248
stroke treatment: maximise reversible ischaemic tissue
ensure hydration
keep oxygen sats >95%
if ischaemia proceed to thrombolysis
249
stroke treatment: thrombolysis
can be given up to 4.5 hours post onset of symptoms
give tissue plasminogen activator- IV alteplase
then antiplatelet therapy- clopidogrel
if time of onset unknown and thrombolysis is unsuitable give aspirin daily for 2 weeks then lifelong clopidogrel
250
stroke treatment: thrombolysis contraindications
```
recent surgery in last 3 months
recent arterial puncture
history or active malignancy
evidence of brain aneurysm
on anticoagulants
clotting disorder
```
251
treatment for haemorrhagic stroke
```
frequent GCS monitoring
antiplatelets contraindicated
reverse all anticoagulants
control hypertension
surgery
```
252
risk management for stroke prevention
platelet treatment- aspirin+ dipyridamole/clopidogrel
simvastatin for cholesterol
AF treatment- warfarin
ramipril for BP
253
TIA differentials
until full recovery- impossible to differentiate from stroke
hypoglycaemia
intracranial lesion
syncope
254
TIA investigations
carotid artery doppler ultrasound to look for stenosis
CT angiography to see extent of stenosis
ECG to look for MI ischaemia or AF
255
TIA investigations: bloods
```
FBC- polycythaemia
ESR raised in vasculitis
Glucose- hypoglycaemia
creatinine
cholesterol
```
256
TIA treatment: ABCD2 score risk of stroke
Age >60= 1
Blood pressure >140/90= 1
Clinical features- unilateral weakness= 2, speech disturbance w/o weakness= 1
Duration of symptoms- >1hr= 2, 10-59mins= 1
Diabetes= 1
score >6 strongly predicts a stroke and should be referred immediately
257
TIA treatment: antiplatelet drugs
aspirin and dipyridamole for 2 weeks, then lower dose
P2Y12 inhibitor long term- clopidogrel
anticoagulant if they have AF or mitral stenosis- warfarin
258
TIA treatment: control risk factors
long term statin- simvastatin
antihypertensives- ace inhibitors, ramipril or angiotensin receptor blocker, candesartan
improve diet
stop smoking
259
subarachnoid haemorrhage
spontaneous bleeding in subarachnoid space- between arachnoid layer of meninges and pia mater
260
subarachnoid haemorrhage: epidemiology
35-65 y/o
| 5% of strokes
261
subarachnoid haemorrhage causes: rupture of saccular aneurysms
80%
e.g. berry aneurysms
rupture in circle of willis @
junction of posterior communicating artery with internal carotid/ anterior communicating w/ anterior cerebral
262
subarachnoid haemorrhage causes: atriovenous malformation
10%
vascular development malformation often with a fistula between arterial and venous systems causing high flow through AVM
and high pressure arterialisation of draining veins
263
subarachnoid haemorrhage: rare causes
bleeding disorder
mycotic aneurysms
acute bacterial meningitis
tumours
264
subarachnoid haemorrhage: risk factors
```
hypertension
known aneurysm
family history
smoking
bleeding disorders
```
265
subarachnoid haemorrhage: pathophysiology
most common cause is ruptured aneurysm
leads to tissue ischaemia
rapid raised ICP as blood acts as space occupying lesion
long term pressure on brain results in deficits
266
subarachnoid haemorrhage: presentation
```
sudden, sever headache
neck stiffness
vomiting
depressed level of consciousness
coma
fixed dilated pupils
double vision
```
267
subarachnoid haemorrhage: differentials
must differentiate from migraine
meningitis
cortical vein thrombosis
268
subarachnoid haemorrhage investigations: ABG
to exclude hypoxia
269
subarachnoid haemorrhage investigations: heat CT
gold standard
detects >90% in first 48 hours
star shaped lesion- blood filling in gyro patterns around ventricles
270
subarachnoid haemorrhage investigations: lumbar puncture
if CT normal but SAH suspected
CSF is uniformly bloody early on
becomes xanthochromic (yellow) after several hours- bilirubin
271
subarachnoid haemorrhage: treatment
neurosurgeon referral immediately
IV fluids to keep cerebral perfusion
administer calcium blocker to reduce vasospasm and so morbidity from ischaemia
272
subarachnoid haemorrhage treatment: endovascular coiling
preferred to surgical clipping since has lower complication rate
promotes thrombosis and ablation of aneurysm
first line treatment where angiography shows aneurysm
273
subarachnoid haemorrhage treatment: surgery
intracranial stents and balloon remodelling for wide-necked aneurysms
274
subarachnoid haemorrhage: complications
rebleeding
cerebral ischaemia due to vasospasm
hydrocephalus due to blockage of arachnoid granulations
hyponatraemia
275
subdural haemorrhage
caused by accumulation of blood in subdural space
between the arachnoid and dura mater
follows rupture of a bridging vein between cortex and venous sinus
276
subdural haemorrhage: epidemiology
most common where patient has a small brain- alcoholics or dementia or babies
277
subdural haemorrhage: pathophysiology
trauma results in bleeding from bridging veins between cortex and venous sinuses
haematoma forms
weeks later it autolyses due to oncotic/osmotic pressure- water is brought into haematoma causing it to enlarge
slow rise in ICP
278
subdural haemorrhage: risk factors
```
traumatic head injury
cerebral atrophy
increasing age
alcoholism
anticoagulation
```
279
subdural haemorrhage: presentation
sleepiness
headache
unsteadiness
signs of raised ICP
280
subdural haemorrhage: differentials
```
stroke
dementia
CNS masses
SAH
extradural haemorrhage
```
281
subdural haemorrhage investigations: CT head
diffuse spreading, hyperdense crescent shaped collection of blood
usually over one hemisphere
282
subdural haemorrhage investigations: MRI head
for subacute haematomas and smaller haematomas
283
subdural haemorrhage: treatment
refer to neurosurgeons- irrigation/evacuation via burr twist drill and burr hole craniotomy
address cause of trauma
284
extradural haemorrhage
collection of blood between dura and bone
| suspect this after head injury and conscious level falls or is slow to improve or there is a lucid interval
285
extradural haemorrhage: aetiology
traumatic head injury resulting in a fracture
286
extradural haemorrhage: risk factors
usually occurs in young adults
| rare <2 y/o and >60 y/o
287
extradural haemorrhage: pathophysiology
mainly temporal or parietal bone
causes laceration of middle meningeal artery
blood accumulates rapidly over minutes-hours between bone and dura
288
extradural haemorrhage: presentation
```
sever headache
nausea
vomiting
confusion
decreased GCS
death due resp arrest if surgical intervention not done fast enough
```
289
extradural haemorrhage presentation: lucid interval
period of time between traumatic brain injury and decrease in consciousness
whilst haematoma is still small and there is still some bleeding
can last several hours
290
extradural haemorrhage: differentials
```
epilepsy
carotid dissection
carbon monoxide poisoning
meningitis
SAH
```
291
extradural haemorrhage investigations: CT head
shows hyperdense haematoma adjacent to skull- biconvex/lense shaped/lemon shaped
292
extradural haemorrhage investigations: skull x ray
may be normal or show fracture lines crossing course of middle meningeal artery
293
extradural haemorrhage: treatment
emergency management
IV mannitol if increased ICP
neurosurgery
294
primary brain tumours: epidemiology
8/100,000
16th most common adult cancer
2nd most common paediatric cancer
295
primary brain tumours: risk factors
```
primary tumours more common in affluent groups
ionising radiation
vinyl chloride
immunosuppression
family history
```
296
primary brain tumours: astrocytomas
most common primary brain tumour- 85-90%
glial cell in origin
graded I-IV
297
primary brain tumours: grade I pilocytic astrocytomas
good prognosis
completely benign
paediatric tumour mainly
298
primary brain tumours: grade II diffuse astrocytoma
prognosis >5yrs
premalignant tumour
nuclear atypia
299
primary brain tumours: grade III anaplastic astrocytoma
prognosis 2-5 years
malignant
active growth
mitosis present
300
primary brain tumours: grade IV glioblastoma multiforme
<1 year
most common phenotype
active growth, mitotic activity and necrosis
very malignant
301
pathways to malignant gliomas: most common
mainly in those <50-60 y/o
initial genetic error is of glucose glycolysis
mutation of isocitrate dehydrogenase I
excess 2-hydroxyglutarate
triggers genetic instability in glial cells and subsequent inappropriate mitosis
302
pathways to malignant gliomas: less common
more common in those >50-60 y/o
no IDH-1 mutation
catastrophic genetic mutation
poor prognosis even for low grade
303
primary brain tumours: oligodendroma
```
most common in 40-50y/o
arise from oligodendrocytes
grow slowly over several years
calcification is common
may have seizures
WHO grade II
all have IDH-1 mutation
```
304
primary brain tumours: ependymomas
arise from ependymal cells
| line ventricles and spinal cord
305
primary brain tumours: meningiomas
more common in older people and women
| benign and arise from arachnoid mater and may grow to a large size
306
primary brain tumours: neurofibromas/schwanomas
solid, benign tumours that arise from schwann cells
| occur principally in cerebellopontine angle
307
primary brain tumours: medulloblastoma
```
WHO grade IV
primitive small blue cell
tumour of cerebellum
in childhood
highly malignant but can respond to excision and chemo
```
308
primary brain tumours: presentation (4 cardinal symptoms)
symptoms of raised ICP
progressive neurological deficit
epilepsy/seizures
lethargy
309
primary brain tumours presentation: raised ICP
progressive headache
drowsiness
vomiting
papilloedema
310
primary brain tumours presentation: raised ICP- papilloedema
```
swelling of optic disc due to obstruction of venous return from retina
loss of crisp optic nerve head margins
venous engorgement
retinal oedema
haemorrhages
```
311
primary brain tumours presentation: progressive neurological deficit
```
depends on region affected
temporal=dysphagia.amnesia
frontal=hemiparesis/personality change/unable to make plans
parietal= hemisensory loss/dysphagia
occipital=contralateral visual defects
cerebellum=DASHING
```
312
primary brain tumours presentation: progressive neurological deficit (DASHING)
```
Dysdiaochokinesis
Ataxia
Slurred speech
Hypotonia
Intention tremor
Nystagmus
Gait abnormality
```
313
primary brain tumours presentation: epilepsy/seizure
sinister when of recent onset
314
primary brain tumours: differentials
other causes of space occupying lesions
| aneurysm, abscess, cyst, haemorrhage, idiopathic intracranial hypertension
315
primary brain tumours investigations: CT/MRI
determine size and location of lesion
| high grade have irregular edges and high growth rates
316
primary brain tumours investigations: biopsy
via skull burr hole
| determines cancer grade
317
primary brain tumours investigations: lumbar puncture
contraindicated when any possibility of a mass lesion- withdrawing CSF may provoke immediate coning
results in brainstem compression as it passes through foramen magnum
318
primary brain tumours: treatment
surgery to remove mass whenever possible
chemo
oral dexamethasone
anticonvulsants for seizures- oral carbamazepine
319
primary brain tumours treatment: chemotherapy for glioma
at same time as surgery and then for 6 weeks post op
| e.g. temozolomide
320
primary brain tumours treatment: oral dexamethasone
most powerful synthetic steroid
rapidly improves brain performance
reduces inflammation and oedema
321
secondary brain tumours: common neoplasms to metastasise to CNS
```
10x more common than primary
non small cell lung cancer
small cell lung cancer
breast cancer
melanoma
GI
renal cell
```
322
secondary brain tumours: treatment
surgery if <75 y/o
radiotherapy
chemo
palliative care
323
pathology of raised intracranial pressure
herniation haemorrhage
tonsillar herniation/coning
local deformity
decreased CSF volume
324
cerebellar disease: ataxia
name given to a group of neurological disorders that affect balance, coordination and speech
325
cerebellar disease: signs and symptoms
```
dysarthria- slurring of speech
dysphagia- difficulty swallowing
clumsiness
intention tremor
unsteadiness
stumbling/falls
nystagmus
limb and gait ataxia
```
326
cerebellar disease: classification of ataxia
congenital ataxia
episodic ataxia- attacks, resolves, reoccurs
autosomal recessive/dominant
sporadic
327
cerebellar disease: autosomal recessive ataxia
ataxia of gait and limb
absent reflectors
complications include diabetes and cardiomyopathy
328
cerebellar disease: autosomal dominant ataxia
most common in UK
slowly progressive with dysarthria, dysphagia and gait ataxia
stats from late 40s-early 50s
329
cerebellar disease: sporadic ataxia
gluten ataxia
| toxic effects
330
cerebellar disease: investigations
cerebrovascular damage
primary tumours
secondary tumours hydrocephalus
MS
331
neurological disorders and psychiatric presentations
cognitive, psychological and behavioural sequelae of CNS disorder depend on:
- tempo of underlying disorder
- site of brain affected
- neurotransmitter system involved
- individual characteristics
332
neurological disorders and psychiatric presentations: tempo
```
acute= trauma, drugs and infections. associated with delirium or confusional state
chronic= dementia
```
333
neurological disorders and psychiatric presentations: site
certain brain regions are associated with particular patterns of psychological and behavioural disturbances
e.g. right hemisphere stroke can give rise to mania
334
neurological disorders and psychiatric presentations: neurotransmitter
memory impairment in alzheimers= acetyl choline depletion
| depression in parkinsons= serotonin, noradrenaline and dopamine depletion
335
neurological disorders and psychiatric presentations: individual characteristics
age, gender, education or prior psychiatric history can affect how brain pathology can give rise to symptoms.
e.g. higher levels of education can protect against alzheimer's
336
inherited neurological disorders: Wilson's disease
disorder of hepatic copper disposition
| presents with personality change, mood disturbance, psychosis and cognitive impairment
337
inherited neurological disorders: acute intermittent porphyria
metabolic disorder of haem
| can give rise to acute psychosis, agitation, mania and depression
338
inherited neurological disorders: neuroacanthocytosis
blood contains misshapen red blood cells
| associated with anxiety, paranoia, depression, obsessive behaviour
339
presentation of inherited neurological disorders: huntington's
```
subcortical dementia
anxiety
depression
personality changes
delusions
apathy
suicidal thoughts
```
340
presentation of acquired neurological disorders: fronto-temporal dementia
```
blunting of emotions
anxiety
egocentricity
compulsive behaviour
neglect of personal appearance
```
341
presentation of acquired neurological disorders: left lobe dysfunction
presents with semantic dementia
progressive word finding difficulty
loss of language comprehension
depletion of conceptual knowledge
342
presentation of acquired neurological disorders: right lobe dysfunction
prosopagnosia- impaired face recognition
| loss of knowledge about people
343
presentation of acquired neurological disorders: vascular
confusional states occur in 1/3 of pts. in acute stroke
| focal behavioural disturbance caused by cerebral ischaemia can mimic functional disorder
344
presentation of acquired neurological disorders: MS
fatigue
depression
mania
psychosis
345
presentation of acquired neurological disorders: HIV associated dementia
apathy
| social withdrawal
346
presentation of acquired neurological disorders: variant creutzfeldt-jakob disease
anxiety or depression
cognitive symptoms develop
varied neurological features including pyramidal, extrapyramidal, cerebellar signs and myoclonus
347
presentation of acquired neurological disorders: hypothyroidism
```
lethargy
impaired cognition
hallucinations
delusions
often paranoid
```
348
presentation of acquired neurological disorders: hyperthyroidism
anxiety
irritability
delirium
psychosis
349
presentation of acquired neurological disorders: pheochromocytoma
chronic anxiety
| paroxysmal dear akin to panic
350
presentation of acquired neurological disorders: neoplastic/paraneoplastic
depression
paranoia
confusion
disorientation
351
presentation of acquired neurological disorders: trauma
delirium
insidious cognitive decline
odd behaviour
352
presentation of acquired neurological disorders: Wernicke's encephalopathy
confusion
ataxia
ophthalmoplegia
353
presentation of acquired neurological disorders: vitamin B12 deficiency
cognitive decline
| organic psychosis
354
somatisation disorders
when physical symptoms are caused by mental or emotional factors
mental or emotional problem is expressed as one or more physical symptom
355
somatisation disorders: somatisation
many physical symptoms from different parts of the body
356
somatisation disorders: hypochondriasis
fear that the minor symptoms may be due to a serious disease
357
somatisation disorders: conversion disorder
a person has symptoms which suggest a serious disease of the brain or nerves such as total loss of vision
they develop quickly in response to stress
358
somatisation disorders: body dysmorphia
a person spends a lot of time worried and concerned about their appearance, focussing on an apparent physical defect that others cannot see
359
somatisation disorders: pain disorder
a person has persistent pain that cannot be attributed to a physical disorder
360
dissociative disorders
a range of conditions that can cause physical or psychological problems
can be short lived, following trauma, and resolve on their own
can last a long time
361
dissociative disorders: of movement or sensation
includes convulsions
paralysis
and loss of sensation
362
dissociative disorders: dissociative amnesia
periods where they cannot remember information about themselves
may forget a learnt skill
363
dissociative disorders: identity disorder
may feel uncertain about their identity and who they are
| may feel presence of other identities
364
spinal cord disease: hemiplegia
paralysis of one side of the body caused by lesion of brain
365
spinal cord disease: paraplegia
paralysis of both legs
| always caused by spinal cord lesion
366
spinal cord disease: upper motor neurone signs
contralateral to lesion
indicate lesion above anterior horn cell
increased muscle tone
367
spinal cord disease: lower motor neurone signs
ipsilateral to lesion
indicate lesion is either in anterior horn cell or distal to anterior horn cell
decreased muscle tone
368
spinal cord disease: spondylolisthesis
slippage of one vertebra over the one below
nerve root comes out above the disc
therefore root affected will be one below disc herniation
369
spinal cord disease: spondylosis
degenerative disc disease
370
spinal cord disease: myelopathy
caused by spinal cord compression
| upper motor neurone signs
371
spinal cord disease: radiculopathy
caused by spinal root compression
lower motor neurone signs
pain down dermatome
weakness in myotome
372
spinal cord compression
compression of spinal cord resulting in upper motor neurone signs and specific symptoms dependent on the location of compression
373
spinal cord compression causes: vertebral body neoplasms
most common cause of acute compression
| secondary malignancy commonly from lung, breast, prostate, myeloma or lymphoma
374
spinal cord compression causes: disc herniation
when centre of disc (nucleus pulposus) has moved through annulus resulting in pressure on nerve root and pain
375
spinal cord compression causes: disc prolapse
when nucleus pulposus moves and presses against the annulus but it doesn't escape outside annulus
can produce a bulge in disc- this results in pressure on nerve causing pain
376
spinal cord compression causes: rare
infection- epidural abscess
haematoma- warfarin
primary spinral cord tumour
377
spinal cord compression presentation: sensory loss below level of lesion
known as the sensory level
| sensation abruptly diminishes 1/2 cord segments below the level of actual anatomical lesion
378
spinal cord compression presentation: L5/S1
S1 nerve root compression= sciatica
| sensory loss/pain in back of thigh/leg/lateral aspect of little toe
379
spinal cord compression presentation: L4/L5
sensory loss/pain in lateral thigh/leg and medial side of big toe
380
spinal cord compression: differentials
```
transverse myelitis
multiple sclerosis
cord vasculitis
trauma
dissecting aneurysm
```
381
spinal cord compression: MRI
do not delay imaging
| identifies the cause and site of compression
382
spinal cord compression: treatment
refer to neurosurgeons
epidural steroid injection
surgical decompression
removal of herniated tissue
383
cauda equine syndrome
medical emergency
| spinal damage at or caudal to L1
384
cauda equine syndrome: epidemiology
rare
| occurs mainly in adults
385
cauda equine syndrome: aetiology
```
common cause is lumbar disc herniation @ L4/5 or L5/S1
tumours
trauma
infection
spondylolisthesis
```
386
cauda equine syndrome: presentation
```
bilateral sciatica
saddle anaesthesia
bladder/bowel dysfunction
erectile dysfunction
variable leg weakness- flaccid and areflexic
```
387
cauda equine syndrome: differentials
conus medullaris syndrome
vertebral fracture
peripheral neuropathy
388
cauda equine syndrome: investigations
MRI to localise lesion
knee flexion test
ankle plantar flexion test
389
cauda equine syndrome: treatment
refer to neurosurgeon asap to relieve pressure
390
parkinson's disease
degenerative movement disorder caused by a reduction in dopamine in substantia nigra
391
parkinson's: epidemiology
increasing prevalence with age
more common in males
peak onset 55-65 y/o
non smokers have higher risk
392
parkinson's: aetiology
```
idiopathic
drug induced
environmental factors
parkinson genes
oxidative stress and mitochondrial dysfunction
```
393
parkinson's: pathophysiology
- substantia nigra usually produces dopamine
- mitochondrial dysfunction results in progressive degeneration of dopaminergic neurones that project into striatum of basal ganglia
- less dopamine means thalamus is inhibited
- a decrease in movement (hence symptoms)
394
parkinson's: presentation
```
onset is usually gradual
impaired dexterity
unilateral foot drop
asymmetrical- one side worse than the others
difficulty with fine movements
speech quiet
drooling of saliva
depression is common
```
395
parkinson's presentation: triad
tremor
rigidity
bradykinesia
396
parkinson's presentation: tremor
```
worse at rest
often asymmetrical
obvious in hands
improved by voluntary movements
made worse by anxiety
```
397
parkinson's presentation: rigidity
as extrapyramidal lesion
increased tone in limbs and trunk
resist passive extension throughout movement
can cause pain
398
parkinson's presentation: bradykinesia/hypokinesia
slow to initiate movement and slow, low-amplitude excursions in repetitive actions
reduced blink rate, monotonous hypophonic speech, write smaller
399
parkinson's presentation: gait
```
reduced asymmetrical arm swing
narrow gait
stooped postured
small steps
shuffling steps, dragging feet
expressionless face
```
400
parkinson's: differentials
```
benign essential tremor
multiple cerebral infarct
lewy-body dementia
drug-induced, trauma
if suspect early parkinson's but: dementia, incontinence, symmetry, early falls. THEN probably not parkinson's
```
401
parkinson's: investigations
clinical diagnosis
| confirm with response to L-DOPA
402
parkinson's: treatment
aim is compensate for loss of dopamine
| physiotherapy for balance, speech and gait problems
403
parkinson's treatment: L-DOPA
gold standar
give alongside decarboxylase inhibitor (co-careldopa) (prevents peripheral conversion of LDOPA, reducing peripheral side effects and maximises dose that crosses BBB)
precursor to dopamine so can cross BBB
404
parkinson's L-DOPA: side effects
```
nausea
vomiting
arrhythmia
psychosis
motor complications
```
405
parkinson's L-DOPA side effects: reduced efficacy
effect wears off in 5-10 years
| so L-DOPA avoided for as long as possible
406
parkinson's L-DOPA side effects: on-dyskinesias
hyperkinetic, choreiform movement when drug works
| repetitive, rapid, jerky, well coordinated, involuntary
407
parkinson's L-DOPA side effects: off-dyskinesias
fixed, painful, dystonic posturing
twisting
caused by sustained repetitive muscle contractions
408
parkinson's L-DOPA side effects: freezing
unpredictable loss of mobility
409
parkinson's treatment: dopamine agonists
oral ropinrole
| used to delay starting L-DOPA
410
parkinson's treatment: monoamine oxidase B inhibitors
oral selegiline
inhibit MAO-B which break down dopamine- so dopamine remains for longer
used to delay starting L-DOPA
411
parkinson's treatment: catechol-O-methyl transferase inhibitors
oral entacapone
| inhibition stops breakdown of dopamine
412
parkinson's treatment: neuropsychiatric complications
depression, dementia, psychosis
SSRI's- citalopram
antipsychotics- quetiapine
413
huntington's chorea
huntington's is a cause of chorea and is a neurodegenerative disorder
lack of inhibitory neurotransmitter GABA
414
huntington's chorea: epidemiology
autosomal dominant condition with full penetrance
| presents middle age
415
huntington's chorea: aetiology
mutation on chromosome 4
| results in repeated expression of CAG sequence
416
huntington's chorea: risk factors
having a parent with Huntington's
| child has 50% risk of getting it
417
huntington's chorea: pathophysiology
repeated CAG leads to translation of expanded polyglutamine repeat sequence
the more CAG is repeated the earlier the onset
progressive cerebral atrophy with marked loss of neurones in caudate nucleus and putamen
specific loss of GABA-nergic and cholinergic neurons
418
huntington's chorea: presentation
```
mild psychotic and behavioural symptoms
dysarthria, dysphagia and abnormal eye movements
apathy
dementia
seizures
chorea
```
419
huntington's chorea: chorea presentation
```
relentlessly progressive, jerky, explosive, rigidity
involuntary movements
ceases when sleeping
can't sit still
may begin as general restlessness
```
420
huntington's chorea: differentials
sydenham's chorea
wilson's disease
SLE
stroke of basal ganglia
421
huntington's chorea: genetic testing
shows how many CAG repeats
| counselling required due to impact of positive diagnosis
422
huntington's chorea: CT/MRI
shows caudate nucleus atrophy and increased size of frontal horns of lateral ventricles
423
huntington's chorea: treatment
no treatment to prevent progression
counselling
antidepressants
risperidone treats aggression
424
huntington's chorea: symptomatic management of chorea
benzodiazepines
sulpiride- neuroepileptic
tetrabenazine- dopamine depleting agent
425
myasthenia gravis
autoimmune disease against nicotinic acetylcholine receptors (AChR) in neuromuscular junction
426
myasthenia gravis: epidemiology
more common in females than males UNTIL over 50 is more common in males
peak age of incidence for women = 30 y/o, males = 60 y/o
427
myasthenia gravis: aetiology/risk factors
in women, associated with other autoimmune disease and thymic hyperplasia
in men it is associated with thymic atrophy or thymic tumour
428
myasthenia gravis: pathophysiology
autoimmune
mediated by antibodies to AChR- interfere with neuromuscular junction via depletion of working post-synaptic sites
achieved by immune complex deposition of anti-AChR IgG and complement at post-synaptic membranes
both T and B cells implicated
blocked excitatory effect- muscle weakness
429
myasthenia gravis: presentation
proximal limb muscles, speech and facial expression are commonly affected
ptosis, diplopia and myasthenic snarl on smiling
resp difficulties
430
myasthenia gravis presentation: muscle groups affected
in order:
- extra-ocular
- bulbar (swallowing/chewing)
- face
- neck
- trunk
431
myasthenia gravis presentation: increasing muscular fatigue
worsened by pregnancy, infection, exercise
to elicit:
-ask to count to 50, their voice becomes less audible
-hold your finger up high, ask to keep looking at it with eyes only, can't keep it up
432
myasthenia gravis: differentials
MS
hyperthyroidism
acute guillain-barre syndrome
lambart-eaton myasthenic syndrom
433
myasthenia gravis investigations: serum anti-AChR
raised in 90%
| if negative then look for muscle specific tyrosine kinase antibodies (anti-MuSK)
434
myasthenia gravis investigations: electromyography and nerve conduction study
EMG detects it as muscle cells not properly activated
| characteristic decrement occurs in evoked muscle action potential during repetitive stimulation
435
myasthenia gravis investigations: CT of thymus
look for hyperplasia/ atrophy/ tumour
436
myasthenia gravis investigations: tensilon test
IV edrophonium given
muscle power increases within seconds
rarely used due to side effects
437
myasthenia gravis treatment: symptom control
anti-cholinesterase - pyridostigmine
| so more ACh remains in neuromuscular junction
438
myasthenia gravis treatment: immunosuppression
prednisolone
| treat relapse or if there's no response to pyridostigmine
439
myasthenia gravis treatment: thymectomy
removal of thymus if onset < 50 y/o and disease not controlled with anti-cholinesterase
440
myasthenia gravis treatment: myasthenic crisis
weakness of the resp muscles during a relapse can be life threatening
monitor FVC
treat with plasmapheresis
441
paresis
impaired ability to move a body part in response to will
442
paralysis
ability to move a body part in response to will is completely lost
443
ataxia
willed movements are clumsy, ill-directional or uncontrolled
444
involuntary movements
spontaneous movement of a body part, independently of will
445
apraxia
disorder of consciously organised pattern of movement or impaired ability to recall acquired motor skills
446
potential sites of damage along motor pathway
```
motor nuclei of cranial nerve
motor neurones in spinal cord
spinal ventral roots
peripheral nerves
neuromuscular junction
muscle
```
447
upper motor neurone signs
```
upper- everything goes up!
increased muscle tone
brisk reflexes
plantars are upturned on stimulation
upper limb extensor muscles weaker than flexor
lower limb=opposite
```
448
lower motor neurone signs
```
lower- everything goes down!
muscle tone reduced
muscle wasting
fasciculation
reflexes depressed
```
449
motor neurone disease
cluster of major degenerative diseases characterised by selective loss of neurones in motor cortex
cranial nerve nuclei and anterior horn cells
450
motor neurone disease: epidemiology
more common in males
median age of onset 60 y/o
often fatal in 2-4 years
451
motor neurone disease: aetiology/risk factors
no established risk factors
| 5-10% familial- mutation in free radical scavenging enzyme (SOD-1)
452
motor neurone disease: pathophysiology
degenerative condition affecting motor neurones-anterior horn cells
cause both UMN and LMN dysfunction but no sensory or sphincter disturbance, never affects movements
453
motor neurone disease presentation: amyotrophic lateral sclerosis
```
UMN and LMN
most common
loss in motor cortex and anterior horn of the cord
split hand sign
cramps common
wrist and foot drop
```
454
motor neurone disease presentation: progressive muscular atrophy
LMN only
present with weakness, wasting and fasciculation
distal muscle before proximal
455
motor neurone disease presentation: progressive bulbar pasty
LMN only
lower cranial nerves and nuclei initially
dysarthria, dysphasia, nasal regurgitation of fluids
LMN lesion of tongue
456
motor neurone disease presentation: primary lateral sclerosis
UMN only
least common
loss of Betz cells in motor cortex
no cognitive decline
457
motor neurone disease: differentials
```
MS
polyneuropathies
myasthenia gravis
diabetic amotrophy
guillain-barre
spinal cord tumours
```
458
motor neurone disease investigations: clinical findings
definite: LMN+UMN signs in 3 regions
probable: UMN+LMN in 2 regions
probable: LMN+UMN in 1 region/UMN in more than 1 region... w/ EMG showing acute denervation in >2 limbs
possible: LMN+UMN in 1 region
459
motor neurone disease investigations: brain/cord MRI
helps exclude structural causes
460
motor neurone disease investigations: lumbar puncture
exclude inflammatory causes
461
motor neurone disease investigations: nerve conduction studies
denervation of muscles due to degenerative of LMN confirmed by EMG
462
motor neurone disease treatment: anti-glutamatergic drugs
oral riluzole
sodium channel blocker that inhibits glutamate release
prolongs life by 3 months
but raises LFTs
463
motor neurone disease treatment: drooling
drooling due to bulbar palsy
| oral propantheline or amitriptyline
464
motor neurone disease treatment: dysphagia
blend food
nasogastric tube
percutaneous catheter gastrostomy
465
motor neurone disease treatment: spasms
oral baclofen
466
guillain-barre syndrome
acute inflammatory demyelinating ascending polyneuropathy
affects peripheral nervous system- schwann cells
follows upper resp tract or GI infection
467
guillain-barre syndrome: epidemiology
more common in males
peak ages= 15-35 y/o and 50-75 y/o
most common acute polyneuropathy
468
guillain-barre syndrome: aetiology
```
campylobacter jejuni
cytomegalovirus
mycoplasma
zoster
HIV
epstein-barr virus
```
469
guillain-barre syndrome: risk factors
history of resp/GI infection 1-3 weeks prior to onset
| vaccinations have been implicated
470
guillain-barre syndrome: pathophysiology
infectious organisms share same antigens as those on schwann cells- leads to autoantibody mediated nerve cell damage
reduction in peripheral nerve conduction follows- acute polyneuropathy
471
guillain-barre syndrome: presentation
- 1-3 weeks post infection, symmetrical ascending muscle weakness
- all limbs then affected, can lead to paralysis
- proximal muscles are more affected- trunk/resp/CN 7
- pain common
472
guillain-barre syndrome: differentials
other causes of acute paralysis:
- hypokalaemia
- stroke
- brainstem compression
- encephalitis
- vasculitis
- myasthenia gravis
473
guillain-barre syndrome: nerve conduction studies
diagnostic if matches clinical examination
| show slowing of conduction, prolonged distal motor latency
474
guillain-barre syndrome: lumbar puncture
done at L4
| CSF has raised protein but normal white cell count
475
guillain-barre syndrome: spirometry
monitors FVC if resp involvement
| decreased FVC indicates the need to admit to ITU
476
guillain-barre syndrome: treatment
ventilate to improve FVC
IV immunoglobulin for 5 days- decreases severity of paralysis
plasma exchange
low molecular weight heparin and compression stockings
477
headache
a symptom of many different illnesses and medications
478
headache classification
primary secondary and other (trigeminal neuralgia/facial pain)
479
primary headaches
no underlying cause
| migraine, cluster and tension
480
secondary headaches
underlying cause
| meningitis, SAH, giant cell arteritis, medication
481
secondary headache red flags
```
HIV or immunosuppressed
fever
thunderclap
seizure
suspected meningitis/encephalitis
```
482
migraines
recurrent throbbing headache often preceded by an aura and associated with vomiting and visual changes
483
migraines: epidemiology
most common cause of episodic/recurrent headache
more common in females
90% onset before 40 y/o
484
migraines: causes CHOCOLATE
```
Chocolate
Hangovers
Orgasms
Cheese
Oral contraception
Lie-ins
Alcohol
Tumult (loud noise)
Exercise
```
485
migraines: risk factors
females
adolescence
genetic component- family history
486
migraines: pathophysiology
- genetics play a role in causing neuronal-hyper-excitability
- changes in brainstem blood flow lead to an unstable trigeminal nerve nucleus in basal thalamus
- self propagating wave spread across cerebral cortex
- release of inflammatory mediators which act on trigeminal nerve nucleus
487
migraines without aura: presentation
```
attacks for 4-72 hours
at least 2 of:
unilateral/pulsing/moderate-severe pain/aggravated by physical activity
during, at least one of:
nausea/vomiting/photophobia
```
488
migraines with auras: presentation
at least 2 attacks
aura precedes attack by minutes
visual= chaotic cascading/jumbling/distorting lines/dots. Black hole in field. hemianopia
tingling/prickling face
489
general migraines: features
at least 2 of:
unilateral pain/throbbing pain/moderate-severe/motion sensitivity
at least 1 of:
nausea/vomiting/photophobia
490
migraines: differentials
tension headache
medication
brain tumour
491
migraines: investigations
mainly clinical
| examine eyes for papilloedema, BP, head and neck
492
migraines: when to perform neuroimaging
```
worst headache/thunderclap
change in pattern
abnormal neuro exam
onset > 50 y/o
epilepsy
```
493
migraines: lumbar puncture investigations
worst headache/thunderclap
rapid onset/progressive
neuroimaging should precede to rule out mass/lesion/raised ICP
494
migraines: acute treatment
NSAIDs- avoid ibuprofen
| triptans- sumatriptan
495
migraines: prevention
if more than 2 attacks/month or acute treatment needed 2x/week
beta blocker- propranolol
amitriptyline
496
tension headaches
most chronic daily and recurrent headaches are tension headaches
497
tension headaches: epidemiology
can be episodic, <15 days/month
| or chronic >15/month
498
tension headaches: aetiology
```
stress
sleep deprivation
hunger
eyestrain
anxiety
noise
```
499
tension headaches: presentation
```
without vomiting
not affected by exercise
tight band sensation
pressure behind eyes
30 mins-7 days
```
500
tension headaches: pain presentation
bilateral
pressing/tight non-pulsatile
mild/moderate intensity
scalp muscle tenderness
501
tension headaches: differentials
migraine
cluster headache
giant cell arteritis
drug induced
502
tension headaches: investigations
clinical diagnosis from history
503
tension headaches: symptomatic treatment
```
aspirin
paracetamol
NSAIDs
no opioids
amitriptyline
```
504
cluster headaches
most disabling headache disorders
505
cluster headaches: epidemiology
rare 1/1000
more common in males
affects adults, 20-40 y/o
common in smokers
506
cluster headaches: risk factors
smoker
male
autosomal dominant gene has a role
507
cluster headaches: pathophysiology
unknown
| may be due to superficial temporal artery smooth muscle, hyper-activity to serotonin
508
cluster headaches: presentation
abrupt onset
excruciating pain around one eye/temple/forehead
facial flushing
miosis/ptosis
pain is strictly unilateral and almost always affects same side
last 4-12 weeks
509
cluster headaches: differentials
migraine
510
cluster headaches: investigations
clinical diagnosis
| at least 5 headaches fulfilling typical presentation
511
cluster headaches: treatment
analgesics unhelpful
| triptan- SC sumatriptan. reduce vascular inflammation
512
cluster headaches: presentation
calcium channel blocker- verapamil
avoid alcohol
corticosteroids may help- prednisolone
513
trigeminal neuralgia
```
CN5= motor and sensory
.1=ophthalmic
.2= maxillary
.3=mandibular
chronic debilitating condition resulting in intense and extreme episodes of pain
```
514
trigeminal neuralgia: epidemiology
peak incidence 50-60 y/o
| more common in females
515
trigeminal neuralgia: aetiology
mainly due to compression of trigeminal nerve by a loop of vein or artery
local pathology= aneurysms, meningeal inflammation, tumours
516
trigeminal neuralgia: fifth nerve lesion causes
w/i brainstem= tumour, MS, infarction
cerebellopontine angle= acoustic neuroma, tumour
petrous bone=spreading middle ear infection
cavernous sinus= aneurysm of internal carotid
517
trigeminal neuralgia: pathophysiology
hypertension
| triggered by washing affected area/shaving/eating/talking
518
trigeminal neuralgia: presentation
compression of the trigeminal nerve results in demyelination and excitation of the nerve resulting in erratic pain signalling
519
trigeminal neuralgia: pain presentation
```
almost always unilateral
3 attacks required
reoccurring in paroxysmal attacks from seconds to minutes
severe intensity
electric shock like
precipitated by innocuous stimuli
```
520
trigeminal neuralgia: differentials
```
giant cell arteritis/temporal arteritis should be excluded
dental pathology
temporomandibular joint dysfunction
migraine
cluster
```
521
trigeminal neuralgia: investigations
need 3 attacks with unilateral face pain
based on history
MRI to exclude secondary causes
