Hersenen Flashcards
(170 cards)
1
Q
Most common cause of radial nerve palsy
A
entrapment at spiral groove
‘Saturday night palsy’
2
Q
presenting symptoms of radial nerve palsy
A
- Wrist and finger drop
- Usually painless
- Motor weakness – mainly the extensors (wrist/finger extension)
Numbness over first dorsal interosseous muscle
3
Q
Most common cause of ulnar nerve palsy
A
Entrapment at ulnar groove (medial epicondyle of humerus)
NB: Cyclists may end up with a problem due to excessive compression on the wrist
4
Q
presenting symptoms of ulnar nerve palsy
A
May be history of trauma at elbow
• Sensory disturbance and weakness “weak grip”
• Usually painless
• Motor weakness - finger abduction/wrist flexion
5
Q
Most common cause of median nerve palsy
A
entrapment within carpal tunnel at wrist
• Pregnancy
• hyperthyroisism
6
Q
presenting symptoms of median nerve palsy
A
History of intermittent nocturnal PAIN, numbness and tingling – often relieved by shaking hand
Patient may complain of “weak grip”
Positive Tinel’s sign/Phalen’s test (Wrist Flexion Test)
Motor weakness
7
Q
Most common cause of Anterior Interosseous Branch (median nerve) palsy
A
Trauma to forearm
8
Q
presenting symptoms of Anterior Interosseous Branch (median nerve) palsy
A
unable to make ok sign
weak grip
history of trauma to forearm
no sensory changes
9
Q
Most common cause of femoral nerve palsy
A
haemorrhage / trauma
May be iatrogenic (femoral lines)
10
Q
presenting symptoms of femoral nerve palsy
A
Not normally painful
Weakness of Quadriceps = knee extension
Weakness of Hip flexion/hip abduction
Numbness in medial shin
11
Q
Most common cause of common peroneal nerve palsy
A
entrapment at fibular head
12
Q
Most common mononeuropathy in the lower limb
A
common peroneal nerve
13
Q
presenting symptoms of common peroneal nerve palsy
A
May be history of trauma, surgery or external compression (crossing of legs)
Acute onset foot drop + sensory disturbance
Usually painless
Motor weakness
NB: Foot drop is a common sign in neurology, but when it comes from Common peroneal nerve, ankle reflexes will be intact and foot inversion is still possible
14
Q
Mononeuritis multiplex
A
painful, asymmetrical sensory and motor peripheral neuropathy
involves isolated damage to at least 2 separate nerves
causes tend to be systemic (DM, vasculitis, CT diseases, lymphoma, infection - Hep C/HIV)
Multiple nerves in random areas of the body can be affected.
15
Q
What does breathlessness on lying flat indicate?
A
Weakness of the diaphragm
Worse on lying flat because the abdominal viscera exert pressure
16
Q
Functions of the peripheral nervous system
A
sensory input to CNS
motor output to muscles
innervation of viscera
17
Q
Causes of length-dependent axonal neuropathy
A
diabetes
alcohol
Folate / B12 / thiamine /B6 deficiency RA, SLE, vasculitis Renal failure, hypothyroidism Drugs Infectious: HIV, hepatitis B & C
18
Q
Guillain-Barré syndrome
A
Acute inflammatory demyelinating neuropathy
Progressive (ascending) weakness. Affects proximal muscles. +/- respiratory / bulbar / autonomic involvement
Flaccid, quadraparesis with areflexia
History of recent infection (campylobacter/EBV/CMV). Trigger infection causes formation of antibodies which attack the myelin sheath
Demyelination will cause conduction block
19
Q
Myasthenia gravis
A
Autoimmune disorder: antibodies to nicotinic acteylcholine receptor at post-synaptic NMJ
May be associated with thymic hyperplasia or thymoma
Affects young women in 20’s and older men in 70’s
Fatiguable weakness of ocular, bulbar, neck, respiratory and/or limb muscles
Antibodies to AChR present in 85% of cases
20
Q
commonest type of peripheral neuropathy
A
Length-dependent axonal neuropathy
21
Q
Which condition presents with ascending flaccid tetraparesis?
A
Guillain-Barré syndrome
22
Q
Which condition is characterised by formation of antibodies against post-synaptic acetylcholine receptor?
A
Myasthenia gravis
23
Q
Primary headache vs Secondary headache
A
Primary headache = headache and its associated features is the disorder (no underlying cause)
• E.g. Migraine, tension-type headache, cluster headache
Secondary headache = secondary to underlying cause
• E.g. Subarachnoid haemorrhage, SOL, meningitis, temporal arteritis, high/low ICP, drug-induced
24
Q
‘Red Flag’ features suggesting secondary headache
A
= SNOOPT
Systemic symptoms
Neurological signs or symptoms (focal/non-focal)
Older age at onset (>50)
Onset is acute (under 5 minutes) = thunderclap
Previous headache history is different / absent
Triggered headache (valsalva or posture)
Assess cranial nerves and fundoscopy
25
Aura
Recurrent reversible focal neurological symptom (eg. visual, sensory, motor)
Develops over 5-20 mins and lasts <60 mins
Visual aura is most common (eg. scotoma, flashing lights, fortification spectrum)
Sensory aura often starts in hand and migrates up arm
26
Migraine presentation
```
Headache:
• commonly throbbing or pulsatile
• Moderate – severe intensity
• Gradual onset, duration 4 –72hrs
• Unilateral in 60%, can radiate
• Aggravated by routine physical activity
```
```
Associated symptoms
• Nausea and vomiting
• Photophobia
• Phonophobia
• Osmophobia
• Mood disturbance
• Diarrhoea
```
27
Medication overuse headache
headache 15+ days per month associated with frequent
| use of acute relief medications
28
Management of migraine
* Avoid triggers
* Reduce caffeine / alcohol intake
* regular meals and sleep patterns
Acute management
• Simple analgesia (Paracetamol, Aspirin, NSAIDs)
• Triptans (eg. Sumatriptan)
• +/- antiemetic (eg. domperidone, metoclopramide)
Prophylaxis
• Beta-blockers (Propanolol)
• Tricyclic antidepressants (Amitriptyline, Nortriptline)
• Anti-epilepsy drugs (Sodium Valproate)
29
Thunderclap headache
abrupt-onset of severe headache which reaches maximal intensity <5 mins (and lasts >1 hr)
“worst headache of life”
“like being hit over the head”
considered as SAH until proven otherwise
```
Other causes:
• Intracerebral haemorrhage
• Arterial dissection (vertebral or carotid)
• Cerebral venous sinus thrombosis
• Bacterial meningitis
```
30
Investigation of thunderclap headache
Aim to identify SAH
```
Bloods
ECG
CT brain
LP - Performed after 12 hours to look for xanthochromia
Intracranial pressure
```
31
xanthochromia
yellow discoloration indicating the presence of bilirubin in the cerebrospinal fluid
32
Raised pressure headaches: features
Worse on lying flat, improved on sitting / standing up
Worse in the morning
Persistent nausea / vomiting
Worse on valsalva (eg. coughing, laughing, straining)
Worse with physical exertion
Transient visual obscurations with change in posture
33
Raised pressure headaches: examination findings
Optic disc swelling – papilloedema
Impaired visual acuity / colour vision
Restricted visual fields / enlarged blind spot
III nerve palsy
VI nerve palsy (false localizing sign)
Focal neurological signs
34
Causes of raised ICP
Mass effect - tumour, oedema, haematoma, abscess
Increased venous pressure - cerebral venous sinus thrombosis, obstruction of jugular venous system
Obstruction to CSF flow / absorption - hydrocephalus, meningitis
35
Low CSF pressure headache features
Headache worse on sitting / standing up and relieved by lying down
Loss of CSF volume causes traction on meninges, cerebral / cerebellar veins and CN V, IX and X
36
Causes of Low CSF pressure
Post-lumbar puncture
Spontaneous intracranial hypotension due to dural tear
37
Stroke
Rapidly developing clinical signs of focal (or global) disturbance of cerebral function, lasting more
than 24 hours or leading to death, with no apparent cause other than that of vascular origin.
objective evidence of focal ischaemic injury in a defined vascular distribution
Anything <24 hours is classified as a TIA
38
Stroke pathophysiology
Always due to a blood clot somewhere, e.g. heart/venous system
Blood clot ascends to the brain through the blood vessels
Blood flow is stopped, and brain becomes starved of oxygen
Neurons are depolarized
Early symptoms -> loss of function. If blood flow is restored at this point, the damage is reversible
Brain tissue dies causing areas of infarction. This is irreversible damage
39
Acute signs/symptoms of stroke
Unilateral weakness: leg/ face & arm/ hemiparesis. body parts affected indicate the location of the lesion due to the differential relative representation on the
motor/somatosensory cortices
Dysphasia
Visual disturbance: e.g. right homonymous heminopia
Acute light-headedness (past-pointing, nystagmus)
40
A stroke can cause expressive or receptive aphasia. Which artery is most likely the blocked one? And which side of the body will likely show motor signs of stroke?
Left MCA
Broca's/Wernicke's are located in the left hemisphere in the majority of people.
Right side of the body will be affected (left motor cortex controls the right side of the body)
41
Definition of ischaemic stroke
An episode of neurological dysfunction caused by focal cerebral, spinal, or retinal infarction.
42
Causes of ischaemic stroke
Cardiac embolism – e.g. AF, heart failure
43
Total Anterior Circulation Syndrome (TACS)
Hemiparesis + Higher cortical dysfunction + hemianopia
Usually proximal MCA or ICA occlusion
Remember: 3H's
44
Partial Anterior Circulation Syndrome (PACS)
o Isolated higher cortical dysfunction OR
o Any 2 of hemiparesis, higher cortical dysfunction, hemianopia
Usually branch MCA occlusion
Remember: Partial, therefore only part (2/3Hs)
45
Posterior Circulation Syndrome (POCS)
Isolated hemianopia OR Brainstem syndrome
Can include perforating arteries, PCA or cerebellar arteries
46
Lacunar Syndrome (LACS)
```
Pure motor stroke
OR pure sensory stroke
OR sensorimotor stroke
OR ataxic hemiparesis
OR clumsy hand-dysarthria
```
Small vessel disease (deep perforating vasculopathy)
47
Definition of intracerebral haemorrhage
A focal collection of blood within the brain parenchyma or ventricular system that is not caused by trauma.
48
Patient presents with new onset expressive dysphasia which he woke up with. What kind of stroke is this?
PACS
49
Patient presents with sudden onset speech disturbance and left-sided weakness 1 hour ago.
O/E: left hemiparesis, left sided hemianopia, left sided neglect
What kind of stroke is this?
TACS
50
Patient presents with sudden onset right sided weakness 5 hours ago.
O/E: hypoasthaesia right face, arm, leg. No movement against gravity in right arm and leg.
What kind of stroke is this?
LACS
51
Patient presents with left sided neck pain since skiing 2/7 ago. Sudden onset vertigo and ataxia yesterday.
O/E: nystagmus, right ptosis, small pupil on right, hypoasthaesia right face, arm, leg, hoarse, right upper limb ataxia
POCS
52
Treatment approach: Ischaemic stroke
IV thrombolysis +/- thrombectomy. Aspirin
Thrombolysis must be within 4.5 hours of onset
Thrombectomy within 6-8 hours. For large vessel disease only
Stroke unit care -> coordinated care, short/long term therapy, prevent aspiration
Hemicranectomy
53
Treatment approach: Haemorrhagic stroke
Intracerebral bleed requires aggressive control of blood pressure
Stroke unit care -> coordinated care, short/long term therapy, prevent aspiration
Neurosurgical evaluation
54
GCS: Eye Opening
4 - Spontaneous
3 - to verbal command
2 - to pain
1 – none
N.B. cannot be assessed if eyes are swollen
55
GCS: Verbal Response
```
5–oriented (T/P/P)
4–confused
3–inappropriate
2–incomprehensible sounds
1–none
```
NB. Append “T” to score if patient is intubate
56
GCS: Motor
```
6 - Obeys commands
5 - Localizes pain
4 - Normal Flexion
3 - Abnormal flexion – looks robotic, slow and unnatural (decorticate)
2 - Extension (decerebrate)
1 – None
```
57
Coma according to GCS
Coma = inability to:
o Obey commands
o Speak
o Open eyes to pain
58
Classification of head injury using GCS
```
Minor = 14-15
Moderate = 9-13
Severe = <8
```
Significance:
consistent strong association between motor score and 6-month Glasgow Outcome Scale (GOS)
GCS and 14-day mortality is ~linear
GCS and 6-month poor outcome is ~linear
59
Most common cause of SAH
trauma
NB: with spontaneous SAH 80-85% are caused by aneurysms.
o 15-20% non-aneurysmal
Tumours
Arteriovenous malformations
Anticoagulant therapy
60
Aneurysmal SAH - Predisposing factors
```
Smoking
Female sex
Hypertension
Positive family history
ADPCK, Ehlers Danlos, coarctation of the aorta
```
61
SAH History
```
Sudden onset (thunderclap) headache
LOC
Seizures
Visual disturbance
speech and limb disturbance
Sentinel headache in 30%
```
62
Clinical examination findings with SAH
```
Photophobia
Meningism - Nuchal rigidity (irritation of the dura)
can present with CHF/pulmonary oedema
Subhyaloid hemorrhages
Vitreous haemorrhages
Speech and limb disturbance
```
63
WFNS grading of SAH
```
Grade I - GCS 15
Grade II - GCS 13-14 without deficit
Grade III - GCS 13-14 with deficit
Grade IV - GCS 7-12
Grade V - GCS 3-6
```
Higher grade = more severe and worse prognosis
64
Investigation- SAH
CT confirms diagnosis and identifies complications
LP: xanthochromia - bilirubin (Takes 6-8 hours post SAH to produce)
If unclear, perform invasive imaging (CTA/DSA)
NB: there may be nonspecific ECG changes and slightly elevated troponin
65
complications of SAH
1) Rehaemorrhage - most common in first 72h
2) Hydrocephalus - due to obstruction of CSF flow
3) Delayed ischaemia - d3-10, due to vasospasm. Give nimodipine
4) Hyponatraemia
5) Cardiopulmonary complications - catecholamine release can lead to myocardial injury (“Stunned Myocardium”)
6) Seizure
7) DVT
66
SAH management
Conservative:
- analgesia
- fluid resuscitation
- nimodipine to prevent Ca dumping and protect against delayed ischaemia
- Anti-embolic stockings due to DVT risk
Surgical
- clipping
- Endovascular stents
67
Seizure
Episode of neuronal hyperactivity causing symptoms and signs (can be localized or can spread)
68
Epilepsy
A syndrome – spectrum of diseases
Characterized by a tendency to have unprovoked seizures
At least two unprovoked episodes of seizure (i.e. it's not epilepsy if they have seizures following head injury)
69
Focal epilepsy
= partial
An area of abnormality in an otherwise normal brain
Causes irritability, causing hypersynchronous discharge,
focal epilepsy can cause either focal or generalized seizures
70
Generalised epilepsy
a generalized tendency towards repeated APs and discharge
usually due to genetic causes - disorder of ion channels/metabolism of neurotransmitters
affects the whole brain at once, causing generalized seizures
71
Focal Epilepsy Features
History of trauma / (ischaemic) birth injury
Focal aura / sequelae
Automatisms
Nocturnal events
Worse post-attack confusion / drowsiness
72
Genetic Generalised Epilepsy (GGE) Features
Photosensitivity
Age of onset = 8-26
Alcohol or sleep deprivation
Myoclonus
Lack of aura (aura = specific area of discharge)
Seizures within 2 hours of awakening - Likely to happen early in the day because GGE is not focal, and therefore there is no build up
Family History in 30%
EEG abnormal
73
Differential diagnosis for first seizure
```
o syncope
o Migraine
o Narcolepsy / cataplexy
o Transient Global Amnesia
o Panic attacks
```
74
Status Epilepticus
>2 seizures without full recovery of neurologic function between seizures
Or continuous seizure activity >30 mins
75
Treatment of focal epilepsy
o Carbamazepine
o Lamotrigine
o Levetiracetam
76
Treatment of generalised epilepsy
o Valproate
o Lamotrigine
o Levetiracetam
77
Multiple Sclerosis
Idiopathic Inflammatory Demyelinating Disease of CNS
results in the destruction of myelin in brain/spinal cord
Acute episodes of inflammation are associated with focal neurological deficits
• usually develop gradually
• last for more than 24 hours
• may gradually improve over days to week
78
Subtypes of MS
Relapsing remitting Multiple Sclerosis
• Most common form
• Attacks initially come and go
• Can develop into secondary progressive MS
Primary Progressive Multiple Sclerosis
• At least 1 year of disease progression
• Gets worse without relapses
Secondary progressive Multiple Sclerosis
• RRMS in past but now progressive disease without relapses
Benign Multiple Sclerosis
79
Syndromes that may develop into MS
1) optic neuritis = inflammation of optic nerve. Causes painful visual loss
2) transverse myelitis = inflammation of spinal cord
3) clinically isolated syndrome = single episode of neurological disability due to focal CNS inflammation
4) radiologically isolated syndrome
80
Multiple sclerosis diagnosis requirements
2 or more episodes of demylination disseminated in space and time
Presence of oligoclonal bands in spinal fluid counts as evidence of dissemination in space and time
NB: It is possible to make the diagnosis of MS with one scan. Evidence of demylination in 2 regions can indicate dissemination in space. If enhancing and non-enhancing areas of demyelination are seen this can indicate dissemination in time (old and new lesions)
81
Causes of MS
unknown - multifactorial
Genetic Factors – there are about 200 risk genes (e.g. vitamin D metabolism genes)
Sunlight/vitamin D exposure
Viral trigger - possibly EBV
Smoking
82
investigation of suspected MS
MRI brain and cervical spine with gadolinium contrast
LP with matched blood sample to look for oligoclonal bands. Bands in CNS only indicated antibody production in CNS
Bloods to rule out differentials - B12/lyme/ANA/ANCA/RF
Visual evoked potentials to detect subclinical optic neuritis
CXR - exclude sarcoidosis
83
MS Relapse Vs. Pseudo-relapse
A relapse usually involves a new neurological deficit that lasts for more than 24 hours in the absence
of pyrexia or infection
A pseudo-relapse is the reemergence of previous neurological symptoms or signs related to an old
area of demylination in the context of heat or infection
84
MS treatment
Treat some relapses with steroids, but this does not affect disease progression, so it's important to weigh up risks/benefits
No licensed DMARD. Some available but bad secondary immune consequences
Biotin supplement may give some symptom relief - gives energy to damaged nerve cells
Mainstay is symptom management
85
Describe the spinal reflex arc
Ia fibre from muscle spindle senses stretching of a muscle
It synapses directly onto two neurons in the anterior horn:
1) an alpha motor neuron - excites the muscle group causing contraction
2) an inhibitory interneuron -> inhibits the antagonist muscle group
86
Parkinson’s disease
Slowly progressing neurodegenerative disorder
Loss of dopaminergic neurons within substantia nigra
Surviving neurons contain Lewy bodies = misfolded protein within the cytoplasm of the cell (neurotoxic)
87
Clinical features – parkinsonism
Remember: Facial TRAPS
Facial = expressionless face
T= tremor (pill-rolling) - predominantly at rest.
R= rigidity (cog-wheel)
A= akinesia. NB: Bradykinesia has two components:
• slowness in initiation of voluntary movement
• progressive reduction in speed and amplitude of repetitive actions
P= posture stooped - due to loss of the reflexes that keep you upright
S=shuffling gait
NB: Asymmetric disorder. Starts and remains worse on one side
88
Non-motor symptoms of PD
Neuropsychiatric:
• Dementia
• Depression
• Anxiety
REM sleep behaviour disorder
Autonomic dysfunction
89
Differential diagnosis of PD
Benign tremor disorders (e.g. essential tremor)
Dementia with Lewy bodies
Vascular parkinsonism
Parkinson plus disorders
Drug-induced parkinsonism/tremor (antipsychotics)
90
Investigation of PD
Diagnosis of PD is largely clinical diagnosis
Bloods to rule out other causes of tremor
CT / MRI brain tends to be normal in PD
Imaging of presynaptic dopaminergic function using DATSPECT => shows loss of DA neurons
91
Drug treatment of PD
* L-dopa
* Dopamine agonists
* MAO-B inhibitors
* COMT- inhibitors
92
L-dopa
Taken up by dopaminergic neurons and decarboxylated to dopamine within presynaptic terminals
Prescribed with dopa-decarboxylase inhibitor
Approx. 50% of patients develop motor complications after 5 years(carbidopa)
93
Dopamine agonists
Ropinirole
Pramipexole
Rotigotine
Apomorphine
Act directly on post-synaptic dopamine receptors (D2)
Increase sensitivity to endogenous dopamine
fewer motor complications than L-dopa
Can cause impulse control disorders (eg. Pathological
gambling, hypersexuality)
94
MAO-B inhibitors
Eg. Selegiline, Rasagiline
Prevents dopamine breakdown by binding irreversibly to monoamine oxidase
Can be prescribed as monotherapy in early disease or as adjunct in later disease
95
COMT inhibitors
Eg. Entacapone, Tolcapone
Inhibiting Catechol-o-methyltransferase results in longer L-dopa half-life / duration of action
Co-prescribed with L-dopa in later disease
96
Nonpharmacological options for PD
Deep brain stimulation of subthalamic nucleus
Treatment option in advanced disease
Surgical implantation of electrodes to stimulate subthalamic nucleus
97
Definition - dementia
Syndrome of progressive global decline in cognitive function
Interferes with the ability to function at work or at usual activities
Represents a decline from previous levels of functioning and performing
Is not explained by delirium or major psychiatric disorder
Severe, acquired and must involve more than one brain region
98
Cognitive History
Remember: MEAL
```
Memory
o repetitive questions or conversations
o misplacing personal belongings
o forgetting events or appointments
o getting lost on a familiar route
```
Executive function
o poor understanding of safety risks
o inability to manage finances
o poor decision-making ability
Apraxia/ Visuospatial
o inability to recognize faces or common objects
o Inability to find objects in direct view despite good acuity
Language
o difficulty thinking of common words while speaking
o hesitations
o speech, spelling, and writing errors
99
MMSE pros/cons
quick and easy
high interrater reliability
insensitive to early impairments
poorly covers executive function
influenced by age/education/SE status
100
Addenbrookes Cognitive assessment pros/cons
More sensitive than MMSE in early disease
covers executive function
more detailed assessment
time consuming
101
Alzheimer’s pathology
Early loss episodic memory = Alzheimer’s disease
Classically starts in temporal lobe
Spreads to parietal and frontal lobes
Logopenic variant aphasia- Impaired single word retrieval
102
Semantic Dementia
type of FTD
characterised by inability to match certain words with their images or meanings
Loss of knowledge about the world including words
103
What type of dementia causes loss of episodic memory?
AD
104
What type of dementia causes loss of semantic memory?
Semantic Dementia
105
What defect causes impaired attention/concentration?
delirium
106
Pupillary Light reflex
Afferent pathway:
1. Action potential generated in optic nerve
2. Axons synapse at right and left pretectal nuclei
Efferent pathway:
3. AP passes to right and left Edinger-westphal nuclei
4. AP conducted along both oculomotor nerves
5. Constriction of:
Pupil being illuminated = direct reflex
Contra lateral pupil = consensual reflex
107
What can cause a Relative Afferent Pupil Defect (RAPD)?
Disease of optic nerve or retina
o E.g. optic neuritis
o Large retinal detachment
Affected eye will initially paradoxically dilate in response to the light
108
How would you demonstrate unilateral optic nerve lesion?
Swinging flashlight test
109
ACCOMMODATION CONVERGENCE RELFEX
Pupil constricts to see distant object and get light rays parallel
Lens accommodation
Convergence of the eyes (contraction of both medial rectus muscles)
110
Meningitis
Inflammation of meninges +/- cerebrum (meningo-encephalitis)
Can be acute or subacute
Can be bacterial or viral. Higher mortality associated with bacterial
111
what are the characteristics of inflammatory CSF?
High WCC
Low glucose compared to blood glucose
High protein count
May be bacterial but patient has had antibiotics, therefore the CSF is sterile
NB: glucose levels will be normal in viral meningitis
112
Meningitis Symptoms and Signs
```
95% will have 2 of:
o Headache
o neck stiffness (only 50%)-> late symptom!
o reduced GCS
o fever
```
Confusion is indicative of cerebritis/encephalitis
Rash – purpuric +/or petechial but macular early on (meningococcal disease)
113
pneumococcus appearance
gram positive diplococcus
remember: Pneumococcus is Positive
114
meningococcus appearance
Gram negative diplococci
115
Risk factors for PNEUMOCOCCAL CNS infection
```
70% underlying disorder:
Middle ear disease
Head injury (CSF leak)
Neurosurgery
Alcohol
Immunosupression (HIV)
```
116
Risk factors for Listeria CNS infection
Transmitted through eating unpasteurised foods, e.g. cheese/pate
Immunosupression
Pregnancy
Listeria causes a subacute meningoencephalitis
117
Pneumococcal Meningitis
focal signs
seizures
VIII palsy
Other signs of Pneumococcal infection:
o CAP
o ENT
o Endocarditis
Bad prognostic outcome
118
Meningococcal meningitis
characteristic rash
| medical emergency
119
When to do a CT (in suspected meningitis)
```
CT before LP if there are signs of raised ICP:
o GCS ≤ 12
o CNS Signs
o Papilloedema
o Immunocompromised
o Seizure
```
Always give ANTIBIOTICS PRE-CT SCAN
120
Treatment of suspected bacterial meningitis
Do not delay starting IV Antibiotics
Treat for Meningococcus/Pneumococcus and HI
- Ceftriaxone penetrates CNS well
If ≥ 60yrs/risk factors for Listeria add IV amoxicillin
If there is a high likelihood of Pneumococcus add steroids (dexamethasone)
121
Meningococcal (secondary) Prevention
Give close contacts secondary prophylaxis
Chemoprophylaxis (Ciprofloxacin or Rifampicin)
knock out the carrier
122
what kind of meningitis are patients with cochlear implants most susceptible to?
pneumococcal
123
Most common cause of Viral Meningitis
enterovirus
124
Management of Viral Meningitis
supportive treatment
Consider acyclovir ONLY if immunocompromised
125
Intra-cerebral TB
Sub-acute (weeks)
CN lesions usual (III, IV, VI, IX)
Require steroids to reduce inflammatory response
Paradoxical worsening usual
126
HIV Brain disease
Consequence of unrecognised/untreated infection and marked immunodeficiency
127
Cryptococcal meningitis
```
seen in immunodeficiency (HIV)
Raised ICP (often require a shunt)
```
May develop blindness and pulmonary/cutaneous lesions
CSF examination:
o India ink
o Cryptococcal antigen (also blood)
o Culture
128
Causes of bacterial meningitis
meningococcus
pneumococcus
haemophilus influenza
TB
129
Which artery supplies areas of the brain associated with speech?
MCA
130
Transient ischaemic attack (TIA)
```
brief episode (<24h) of neurological dysfunction due to a temporary focal cerebral/retinal ischaemia
without infarction
```
e.g. a weak limb, aphasia or
loss of vision, usually lasting seconds or minutes
with complete recovery.
131
What is the most common type of stroke?
Ischaemic stroke (85%)
Usually caused by thromboembolic disease secondary to atherosclerosis.
Usually a problem with the anterior (carotid) circulation = TACS/PACS/LACS
Posterios circulation (vertebrobasilar arteries) causes POCS
132
Haemorrhagic Stroke subtypes
Intracerebral haemorrhage
Subarachnoid haemorrhage
either a brain aneurysm burst or a weakened blood vessel leak. Blood spills into or around the brain and creates swelling and pressure, damaging cells and tissue in the brain.
133
Most common site of a berry aneurysm
Anterior communicating artery
134
“bulbar weakness”
= weakness of the cranial nerves from the medulla
cranial nerves 9, 10, 11, 12
Gives rise to dysarthria (difficulty speaking) and dysphagia because they supply muscles of the oropharynx
135
What is the natural direction of the eyes?
The orbits naturally point the eyes laterally and superiorly
136
Diplopia
Patient will complain of diplopia (double vision) if one of the cranial nerves isn’t working
Diplopia is worsened by looking in the direction of action of the muscle innervated by that nerve
137
Abducens nerve palsy
prevents the affected eyeball from moving laterally beyond the midpoint
The eyeball usually is directed medially.
This leads to strabismus (crossed eyes) and diplopia.
Can be a nonspecific sign of raised ICP (forced localizing sign)
Images become separated horizontally
138
Internuclear ophthalmoplegia (INO)
Midbrain lesion
Commonly seen in multiple sclerosis
causes failure of adduction of affected eye and nystagmus in the contralateral eye (only during
abduction)
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Herpes zoster ophthalmicus
* Affects CN V1 division
* Pain may precede vesicles
* Elderly and immuno-compromised at risk
* Treated with oral aciclovir
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How can you distinguish clinically between a LMN cause and UMN cause of the facial palsy?
a patient with forehead sparing (i.e. no involvement to the occipitofrontalis muscle) will have a UMN origin to
the palsy, due to the bilateral innervation of the forehead muscle).
LMN will affect the entire half of affected side of face
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hypoglossal palsy
Muscles push the tongue out, so if they are not functioning, the tongue deviates towards the sign of the lesion
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ROSIER score
used to distinguish between suspected stroke and stroke mimics
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Stroke Ddx
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Head injury
Hypoglycaemia
Subdural haemorrhage
Intracranial tumour
Hemiplegic migraine
```
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Causes of haemorrhagic stroke
o CNS bleeds from trauma
| o Ruptured aneurysm
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Causes of ischaemic stroke
o Small vessel occlusion
o Atherothromboembolism
o Cardiac emboli
o Emboli secondary to AF
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Which tests would you request in a suspected stroke?
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Bloods to check fitness for thrombolysis:
FBC -> platelet count crucial
U&Es
CRP/ESR
LFTs
Coagulation profile
```
Glucose -> exclude hypoglycaemia
Lipid profile -> assess risk
CT brain
ECG - to look for ischaemic changes or rhythm abnormalities e.g. AF
CT angiogram to identify the site of occlusion
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What is the role of imaging in acute stroke?
Exclude mimics (tumours, subdural haematoma)
Distinguish ischaemic from haemorrhagic stroke
o Used to rule out a bleed
Identify site of thrombus (CTa and MRa)
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ischaemic penumbra
MRI
region with reduced blood flow (seen on perfusion scan) but no lesion on diffusion weighted imaging (DWI)
presumed to be ‘at risk’ but ‘potentially salvageable’
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What kind of stroke would proximal occlusion of the left MCA cause?
TACS
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Which drug is used for intra-venous thrombolysis (IVT)?
Alteplase
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Mechanisms of Cell Death after Stroke.
Initial ischaemia (reversible) followed by infarction (irreversible damage)
1) excitotoxity
2) peri-infarct depolarization
3) oxidative stress
4) inflammation
5) apoptosis
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Secondary stroke prevention
A - antiplatelet -> aspirin + clopidrogrel
B - BP control -> ACEi + thiazide diuretic
C - cholesterol -> statin
D - diabetes control
```
depending on patient deficit:
Physiotherapy
Speech therapy/swallowing assessment
Occupational therapy
Smoking cessation
Dietician
```
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A patient who is on secondary stroke prevention medication has AF. What do you do?
Assess need for anticoagulant therapy using CHA2DS2VASC score. Give therapy to scores of 2+
use HAS-BLED score to calculate risk of major bleed.
STOP ANTI-PLATELET THERAPY if you give anticoagulant
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incidence, prevalence and economic burden of stroke
commonest neurological disorder and cause of disability worldwide.
accounts for 1 in 18 deaths in western countries.
3rd most common cause of death
consumes 5% of the entire NHS budget
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Stroke signs and symptoms
sudden onset focal CNS signs
Facial asymmetry
Arm/leg weakness (contralateral hemiparesis)
Speech difficulty - slurred, aphasia/dysphasia
Visuospatial neglect
Contralateral homonymous hemianopia
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Uhthoff’s phenomenon
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o Heat (exercise) causes worsening of nerve function
o This is seen in demyelination.
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optic neuritis presentation
pain on eye movement and visual blurring associated with rapidly decreased central vision
can manifest as red desaturation.
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Outline a strategy for the diagnosis of MS
clinical diagnosis based on clinical history supported by examination findings and investigation results.
Exclude mimics (bloods and MRI brain + spinal cord)
Supporting investigations:
MRI findings
LP -> inflammation in CSF (positive oligoclonal bands)
other evidence which may represent demyelination such as abnormal visual evoked responses
(VERS).
The diagnosis of MS is made when we demonstrate two neurological lesions are disseminated in space
and time.
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MS Ddx
sarcoidosis
Lyme disease
B12 deficiency
vasculitis
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What are VERS?
Visual evoked responses
measure the speed at which impulses travel along the optic nerve.
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What form of imaging would you use to show demyelination?
Demyelination shows up as white lesions on T2 MRI
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What treatment options exist in progressive MS?
Treatment options in progressive MS are directed at symptom control.
There is currently no way of reversing damage to the nervous system or stopping progressive disease.
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clinical features of raised intracranial pressure:
Papilloedema
Constriction of visual fields;
Enlargement of the blind spots;
VIth nerve palsy - may be a false localising sign
reduced GCS
Pain
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What investigations would you perform for suspected migraine?
Blood tests
Neuroimaging - Not indicated. may demonstrate incidental abnormalities -> unnecessary anxiety
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Migraine Ddx
tension-type headache
trigeminal autonomic cephalgias (eg cluster headache).
tension-type headache is usually featureless (no nausea, not aggravated by physical activity)
trigeminal autonomic cephalgias are unilateral and associated with prominent ipsilateral cranial autonomic features.
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Discuss the pathogenesis of migraine
considered a neurovascular disorder.
probably dysfunction in sensory brainstem nuclei.
pain results from interactions between components of the trigeminovascular system:
1. The pain-sensitive cranial blood vessels;
2. The trigeminal nerve fibres that innervate them; and
3. The cranial parasympathetic outflow.
aura phase is associated with reduction of blood flow in contralateral hemispheric regions
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differential diagnosis for thunderclap headache
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SAH;
Intercerebral haemorrhage;
Cerebral venous sinus thrombosis;
Arterial dissection (vertebral or carotid);
Bacterial meninigitis;
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risk factors for subarachnoid haemorrhage
Modifiable:
o smoking
o hypertension
o alcohol excess
Non-modifiable:
o previous SAH
o polycystic kidney disease
o connection tissue disease (Ehler’s Danlos, Marfan)
o arteriovenous malformations
o strong family history (>2 first-degree relatives)
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‘surgical’ IIIrd nerve palsy.
IIIrd nerve palsy with dilatation of the pupil
This is because the parasympathetic fibres that supply pupillary constrictor muscles run along the outside of the IIIrd nerve and are subject to compression from ‘surgical’ causes (eg tumour or aneurysm).
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isolated, complete IIIrd nerve palsy with dilatation of the pupil
due to an aneurysm of the posterior communicating artery until proven otherwise.
