Neurology Flashcards
1
Q
Describe the main functions of the brain lobes, cerebellum and brainstem
A
Frontal: movement and executive function
Parietal: sensory
Temporal: hearing, smell, memory, languages, facial recognition
Occipital: vision
Cerebellum: muscle coordination, balance
Brainstem: HR, BP, breathing, GI function, consciousness
2
Q
Which parts of the brain are supplied by the anterior cerebral artery?
A
Medial frontal and parietal
3
Q
Which parts of the brain are supplied by the posterior cerebral artery?
A
Mainly occipital, some temporal and thalamus
4
Q
Which parts of the brain are supplied by the middle cerebral artery?
A
Lateral portions of the frontal, temporal and parietal lobes
5
Q
Where are the most common sites for atherosclerosis in the brain?
A
Branch points, particularly of the internal carotid and middle cerebral
6
Q
Describe a lacunar stroke and it’s causes
A
Hyaline arteriosclerosis of the deep MCA branches leads to protein-filled cyst formation in the brain
Caused by HTN and diabetes
7
Q
What is a watershed infarct?
A
Area of the brain damaged that is at the border of two blood supplies
8
Q
How does cytotoxic oedema occur as a result of an ischaemic stroke?
A
No glucose and oxygen so no energy
High sodium and calcium in the cells draws water in via osmosis
9
Q
How do high calcium levels in the brain cells cause damage in an ischaemic stroke?
A
High Ca2+ causes a buildup of ROS which damage lipids in the mitochondria and lysosomes
Release of apoptosis-releasing factors and digestive enzymes
10
Q
What is the major risk if inflammation damages the blood-brain barrier in an ischaemic stroke?
A
Vasogenic oedema which has a mass effect and pushes into the other side, can causes cingulate/ uncle herniation
If cerebellar tonsil herniation it may compress the brainstem causing breathing problems and reduced consciousness
11
Q
Give two symptoms of an anterior/ middle cerebral artery ischaemia
A
Numbness
Muscle weakness
12
Q
How would an ischaemic stroke affecting Broca’s area present?
A
Slurred speech
13
Q
How would an ischaemic stroke affecting Wernicke’s areas present?
A
Difficulty understanding speech
14
Q
How would you diagnose an ischaemic stroke?
A
Flair MRI
CT scan
Angiography
15
Q
How would you treat an ischaemic stroke?
A
Thrombolytic enzymes: tissue plasminogen activator (TPA)
Aspirin: prevents more clots
Surgery: mechanical embolus removal in cerebral ischaemia (MERCI)
Suction removal
16
Q
How could you minimise risk factors of an ischaemic stroke?
A
Quit smoking Healthy BP Normal cholesterol Control of diabetes Surgery Carotid endarterectomy Stent
17
Q
How can HTN cause an intracerebral haemorrhage?
A
Micro aneurysms (Charcot-Bouchard aneurysms) Hyaline arteriolosclerosis (arteries are still and more likely to rupture)
18
Q
Give 4 conditions associated with intracerebral haemorrhage
A
Arteriovenous malformations
Vasculitis
Vascular tumours
Cerebral amyloid angiopathy (protein deposits in the walls of arterioles making them less compliant)
19
Q
How can an intracerebral haemorrhage occur as a result of ischaemic stroke?
A
Brain tissue death due to ischaemia, if there is reperfusion damaged cells may rupture causing a haemorrhage / haemorrhagic conversion (bleeding into dead tissue)
20
Q
Where might herniation occur in an intracerebral haemorrhage?
A
Falx cerebri
Tentorium cerebelli
Foramen magnum
21
Q
How would you treat an intracerebral haemorrhage?
A
Medication: anti-hypertensives and to relieve ICP
Surgery: craniotomy (relieving ICP and draining blood)
Sterotatic aspiration (CT and needle)
22
Q
Where is CSF found within the meninges?
A
Subarachnoid space
23
Q
Give 3 causes of a subarachnoid haemorrhage
A
Traumatic injury
Aneurysms (saccular cerebral/ berry aneurysms)
Genetic disorders: Marfan syndrome can predispose people
Can rupture with increased ICP
Arteriovenous malformation
24
Q
Describe the consequences of a subarachnoid haemorrhage
A
Pressure on the skull, brain tissue and blood vessels
Arteries bathing in a pool of blood can start to intermittently vasoconstrict/ vasospasm
In circle of Willis there is reduced blood to the brain
Blood irritates the meninges causing inflammation and scarring of surrounding tissue, this can obstruct CSF and cause dilation of the ventricles (hydrocephalus) which increases ICP
25
Give 4 symptoms of a subarachnoid haemorrhage
```
Thunderclap headache
Nuchal rigidity
Seizures
Vomiting
Vision changes
Confusion
```
26
How would you diagnose a subarachnid haemorrhage?
CT
MRI
Lumbar puncture (red blood: fresh/ yellowish blood (bilirubin): old)
27
How would you treat a subarachnoid haemorrhage?
Emergency surgery: clip artery and apply pressure
Use catheter to insert coil to promote clot formation
Medication: CCB to prevent vasospasms
28
Give the diagnostic criteria for a TIA
<24 hours of symptoms, no evidence of infarct on imaging
29
Describe an extra/ epidural haemorrhage
Bleeding that occurs between the skull and dura mater
30
Give 4 causes of an epidural haemorrhage
Trauma
Motor vehicle accident
Falls
Assault
31
What percentage of epidural haemorrhages include a skull fracture?
70-95%
32
Describe the clinical manifestation of an epidural haemorrhage
```
Altered consciousness
Headache
Vomiting
Confusion/ seizures
Aphasia
Pupil asymmetry
```
33
How would you diagnose an epidural haemorrhage?
CT/ MRI:lens shaped lesion, well circumscribes
| X-ray: may show fractures of the skull
34
Which investigation is contraindicated in an epidural haemorrhage?
Lumbar puncture
35
How would you treat an epidural haemorrhage?
Urgent decompression
ABCD, high flow oxygen
Sit up in bed
Neurosurgery: blood is evacuated
36
Describe epilepsy
Recurring and unpredictable seizures, neutrons are synchronously active
37
Give the main excitatory neurotransmitter in the brain and the primary receptor
Glutamate
| NMDA (Ca2+ enters)
38
Give the main inhibitory neurotransmitter in the brain and the primary receptor
```
GABA
GABA receptor (Cl- enters)
```
39
Give 3 ways in which the excitatory and inhibitory receptors in the brain can be affected
Tumours
Brain injury
Infection
40
Describe a focal seizure without impaired awareness
One hemisphere/ lobe affected
Strange sensations, jerking movements
Jacksonian march: starts in one group, spreads
Awake/ alert, often remembers
41
Describe a focal seizure with impaired awareness
Focal seizure with loss of awareness or responsiveness
| May not remember
42
```
Describe the following generalised seizures:
Tonic
Atonic
Clonic
Tonic-clonic
Myoclonic
Absence
```
```
Stiff/ flexed, fall back
Relaxed, fall forward
Convulsions
2 phases
Short muscle twitches
"Spaced-out"
```
43
Describe status epilepticus
If seizure lasts longer than 5 minutes, is ongoing/ without returning to normal (usually tonic-clonic)
Often treated with benzodiazepines which enhance GABA
44
Give 2 main post-seizure symptoms
Postictal confusion
Paralysis (Todd's paralysis: arms and legs)
Lasts around 15 hours, temporary and severe suppression of seizure-affected brain area
45
How would you diagnose epilepsy?
Imaging to look for abnormalities (MRI, CT)
| EEG
46
How would you treat epilepsy?
```
Daily medication:
Anticonvulsants
Epilepsy surgery- remove cause
Vagus nerve stimulation
Ketogenic diet
```
47
Describe Parkinson's disease
Degeneration of dopamine-producing neutrons of the substantia nigra causing a progressive movement disorder
48
Give the two genes in which a mutation may cause Parkinson's
PINK1, PARKIN
49
Give 2 risk factors for Parkinson's
Pesticide exposure
| Genetic variants
50
Describe the substantia nigra and it's function
Part of basal ganglia that connects to the motor cortex and controls movement
51
What is the feature found in neutrons before they die in Parkinson's disease?
Lewy bodies (eosinophilic, alpha-synuclein)
52
Which part of the substantia nigra is affected in Parkinson's disease?
Pars compacta
53
What does the nigrostriatal pathway connect and what is it's purpose?
Substantia nigra to striatum (caudate and putamen)
| Helps stimulate cerebral cortex to initiate movement
54
Describe the motor clinical features of Parkinson's
Resting tremor
Rigidity, stooped posture, almost expressionless
Postural instability
Bradykinesia, hypokinesia, akinesia (difficulty initiating movement) : legs freeze up, shuffling gait
55
How does Parkinson's differ from motor cortex/ corticospinal pathway diseases?
No weakness in Parkinson's
56
Give 4 non-motor symptoms of Parkinson's
Depression
Dementia
Sleep disturbances
Difficulty smelling
57
Why can Parkinson's not be treated with dopamine?
Dopamine cannot cross the blood-brain barrier
58
What would the first line of Parkinson's treatment be and why might side effects be seen?
Levodopa (dopamine precursor) can cross the BBB and is then converted to dopamine by dopa decarboxylase
Peripheral dopa decarboxylase may convert Levodopa before it crosses the BBB and then produce epinephrine which can cause arrhythmias
59
Which drug would you give with L-dopa to prevent side effects?
Carbidopa: dopa decarboxylase inhibitor that cannot cross the BBB
60
How would you treat Parkinson's other than L-dopa?
Amantadine (antiviral that increases dopamine production)
Dopamine agonists: bromocriptine, pramipexole
Inhibitors of COMT (COMT degrades dopamine): entacapone, tolcapone
Since a loss of dopamine increases relative acetylcholine: anticholinergics- improve tremors: benzotropine
61
Give examples of other diseases in which Parkinsonism may be seen
Lewy body dementia
Wilson disease
Pick disease
62
Give examples of medications which may cause Parkinsonism as a side effect
Antipsychotics (haloperidol: blocks dopamine receptors)
| Metoclopramide (dopamine antagonist, anti-emetic)
63
Describe multiple sclerosis
Demyelinating disease of the central nervous system
64
Which cells produce myelin in the CNS?
Oligodendrocytes
65
Describe the chain reaction as T cells are activated by myelin in multiple sclerosis
Stimulates the BBB to express more T-cell receptors and allow more immune cells to cross
T-cells release cytokines which dilate blood vessels so more immune cells can cross the BBB
Cytokines attract B cells and macrophages which produce antibodies against myelin sheath proteins, oligodendrocytes are engulfed and destroyed leaving behind areas of scar tissue
66
Give 2 genetic and 2 environmental risk factors for multiple sclerosis
Female, genes encoding for (HLA-DR2)
Infections, vit D deficiency
67
Describe the following patterns of MS
Relapsing-remitting
Secondary progressive
Primary progressive
Progressive-relapsing
68
Describe the 3 components of Charcot's neurological triad
Nystagmus: plaques in nerves of eyes, involuntary rapid eye movements, loss/ blurred vision, pain/ double vision
Intention tremor: plaques along motor pathways, muscle weakness and ataxia
Dysarthria: plaques in brainstem, difficult/ unclear speech
Interfere with conscious movements, unconscious (swallowing)
69
Describe the symptoms that would result from plaques in sensory pathways in MS
Numbness
Pins and needles
Paresthesias
70
What is Lhermitte's sign (in MS)?
Electric shock that runs down back and radiates to limbs when bending the neck forward
71
Describe the symptoms that would result from plaques in the autonomic nervous system in MS
Bowel/ bladder symptoms
| Sexual dysfunction
72
How would you diagnose MS?
MRI: white matter plaques
CSF: high levels of antibodies
Visual evoked potential: measures response to visual stimuli
73
How would you treat MS?
RRMS:
Medications: corticosteroids, cyclophosphamide, IV Ig
Plasmapheresis: remove autoantibodies
Immunosuppressants: recombinant B-INF, decreased release of inflammatory cytokines in the brain and increased T-reg cells
Progressive MS:
Manage symptoms
Physical therapy
CBT
74
Describe the components making up CSF
70% lymphocytes
30% monocytes
Proteins and glucose
(Pressure 15mmHg/ 100-180mmH20)
75
What is the normal total CSF volume and how much is produced each day?
150ml total
| 500ml produced/ day
76
Describe meningitis
Inflammation of the leptomeninges (arachnoid, pia mater)
77
Give 3 inflammation triggers for meningitis
Autoimmune disease
Adverse reaction to medication: Intrathecal therapy (injected directly into CSF
Infection: Neisseria meningitidis, Herpes simplex
78
How can meningitis arise from direct spread of infection?
Through overlying skin
Through nose
Anatomical defect: spina bifida/ skull fracture
79
How can meningitis arise from haematogenous spread of infection?
Binding to surface receptors
Areas of damage
Vulnerable spots e.g Choroid plexus
80
What is the normal volume of WBCs in the meninges?
5 WBC/mm3
81
Which type of meningitis has a particularly high percentage of PMNs?
Bacterial
82
Which type of meningitis has a particularly high percentage of lymphocytes?
TB meningitis
83
Which type of meningitis can you see the highest volume of WBCs?
Viral
84
How do pressure, glucose conc and protein levels change in meningitis?
Pressure increases, glucose conc decreases, protein levels increase
85
Give the common bacterial causes of meningitis in newborns, children and adults
Newborns: Group B strep, E.coli, Listeria
Children: Neisseria meningitidis, strep pneumoniae
Adults: strep pneumoniae, listeria monocytogenes
86
Give a cause of tick-bourne meningitis
Borrelia Burgdoferi (cause of lyme disease)
87
Give 5 viral causes of meningitis
```
Enterovirus
Herpes simplex
HIV
Mumps
Varicella zoster
```
88
Give 2 fungal causes of meningitis
Cryptococcus genuses
| Coccidioids genuses
89
Give a cause of parasitic meningitis
P. falciparum
90
Give 5 symptoms of meningitis
```
Headache
Fever
Nuchal rigidity
Photophobia
Phonophobia
```
91
What is Kerning's sign?
Lay on back, knee at 90 degrees, pain in back
92
What is Brudzinski's sign?
Lay on back, head lifted, knees bend
93
How would you diagnose meningitis?
Lumbar puncture: needle between L3 and L4, takes CSF, measure pressure, analyse WBCs, protein and glucose
PCR: look for HIV, enterovirus, HSV, TB
94
How would you treat meningitis?
Cause-dependent
Bacterial:
Steroids (to prevent injury to leptomeninges: dexamethasone)
Drugs: anti-vitals, bacterials, fungals, parasitics
Vaccine: Neisseria meningitidis, disseminated TB
Prophylactic Abx
95
Give 4 causes of secondary headaches
Sub-arachnoid
Medication induced
Infection: meningitis
Giant cell arteritis
96
Give 5 red flags accompanying headaches that may indicate a brain tumour
Cluster headaches
Seizures
New onset headache (associated with a Hx of cancer)
Significantly altered consciousness, memory, confusion, coordination
Papilloedema
97
Describe the symptoms and pattern of a migraine
```
4-72 hours
Unilateral, pulsing, worse with activity
Moderate to severe
Nausea and vomiting
Photophobia and phonophobia
```
98
Which factors may worsen a migraine?
```
Cheese
Hangover
Orgasm
Chocolate
Oral contraceptive
Lie in
Alcohol
Tumult
Exercise
```
99
Describe the symptoms and pattern of a tension headache
```
30mins-7 days
Mild-Moderne
Bilateral
Pressing/ tightening
Not aggravated by physical activity
Photo/ photophobia
NO nausea/ vomiting
```
100
Describe the symptoms and pattern of a cluster headache
```
Most severe pain
Unilateral orbital/ suborbital
15-180 minutes
Sense of restlessness/ agitation
Frequent
```
101
How would you treat a migraine?
Triptan and NSAID/ paracetamol
| Anti-emetic
102
How can a medication overuse headache occur?
Underlying headache disorder
Frequent use of analgesics
Rebound headaches occur usually daily
Become chronic daily headaches
103
Give 4 medications which commonly cause overuse headaches
Triptans
Ergotamines
Analgesics
Opioids
104
Give the 2 other possible names for motor neurone disease
Amyotrophic lateral sclerosis
| Lou Gehrig's disease
105
Describe how ALS is classified by onset
Limb onset: upper and lower motor neurone death, limbs affected first
Bulbar onset: motor neurons in the medulla oblongata die first with lower motor neurons
Muscles in the face, mouth and throat are affected first
Faster progression and poorer prognosis
106
How would limb onset ALS present compared to bulbar onset ALS?
Limb: "dropped foot", awkwardness running
Bulbar: slurred speech, dysphagia, dysphasia
107
Describe the general symptoms of motor neurone disease
Muscle cramps, dysphagia, dysarthria, hyperreflexia, spasticity, Babinski's sign, muscle weakness
Late stages: difficulty chewing/ swallowing: increased risk of aspiration
Decreased strength of intercostals: loss of lung function
108
Give 2 possible causes/ risk factors of ALS
Genetics
Head injury
(90% no FHx)
109
How would you manage motor neurone disease?
```
Riluzole: protects motor neurone by reducing activity (prolongs survival)
Medications to control symptoms:
Baclofen and diazepam
Glycopyrrolate (trouble swallowing saliva)
Analgesics
Breathing support
Therapy
Nutritional advice
```
110
Describe the differences between UMN lesions and LMN lesions
```
UMN: Damage anywhere along corticospinal tracts
weakness affects groups
spasticity
Increased tone
Hyperreflexia
+ve Babinski sign
```
LMN: Damage anywhere from the anterior horn cells distally
Affected muscles show wasting and fasciculation
Hypotonia/ flaccidity
Reflexes are reduced/ absent
111
Give 3 symptoms of autoimmune encephalitis
Catatonia
Psychosis
Abnormal movements
112
Give 4 causes of viral encephalitis
Herpes simplex
Rabies
Poliovirus
Measles
113
Give 3 causes of bacterial encephalitis
Syphilis
Meningitis
Malaria (immunocompromised)
114
Give 4 symptoms of limbic encephalitis
Disorientation
Disinhibition
Memory loss
Seizures
115
Give 4 general symptoms of encephalitis
Fever
Headache
Confusion
Seizures
116
How would you diagnose encephalitis?
```
MRI
EEG
Lumbar puncture
Blood test
Urinalysis
```
117
How would you treat encephalitis?
```
Antiviral medication
Abx
Steroids to reduce swelling
Sedatives for restlessness
Acetaminophen for fever
```
118
How might herpes zoster virus present?
Chicken pox: fever, malaise headache, abode pain
Rash: pruritic, erythematous, crust (infectious 1-2 days pre and 5 days post-rash development)
Shingles: painful, hyper-aesthetic area, then macular becomes a vesicular rash
May become a disseminated infection if immunosuppressed
119
How would you treat herpes zoster virus infection?
Oral aciclovir/ valaciclovir (within 48 hours of rash)
| IV aciclovir if pregnant/ immunosuppressed
120
What percentage of childhood tumours are brain tumours?
20%
121
In general, where are brain tumours found in adults and where in children?
Adults: supratentorial compartment
Children: infratentorial compartment
122
How might a brain tumour present?
```
Cluster headaches
Papillary oedema
Focal deficits
Seizures: olfactory aura and deja vu
Loss of function
Drowsiness
Nausea/ vomiting
```
123
How might brain tumours be classified according to cells affected?
```
60% neuroepithelial: astrocytic/ oligodendritic
7% cranial/ spinal nerve tumours
28% meningeal
4% lymphomas
1% germ cell tumours
```
124
What is the WHO grading system for brain tumours?
Grade 1: Pilocytic astrocytoma (benign)
Grade 2: Diffuse astrocytoma (pre-malignant: 5-7 year prognosis)
Grade 3: Anaplastic astrocytoma (2-5 year prognosis)
Grade 4: Glioblastoma, most common type (<1 year prognosis)
125
Which mutations are associated with an astrocytoma and an oligodendroglioma?
Astrocytoma: IDH1 mutant
Oligodendroglioma: IDH1 and 1P 19Q mutant
126
Describe a medulloblastoma
WHO grade 4 most commonly
"Small blue tumour" of the cerebellum
Common in childhood
Rapidly fatal if untreated
127
Where are the common sites of brain metastases?
```
Lung
Breast
GI
Kidney
Melanoma
```
128
How would you treat a brain tumour?
Aggressive surgery if possible
| Radiotherapy with adjuvant chemo (Temozolomide)
129
Give 4 causes of spinal cord compression
Tumour
Vertebral fracture
Abscess
Ruptured intervertebral disc
130
How might tumours grow within the spinal cord?
Causing vertebral displacement (mass effect on cord)
Tumours can grow para-spinally into the foramen
Epidural: between the disc then superiorly and inferiorly
131
Describe the 4 symptom groups of spinal cord compression
Back pain: first symptom, progressively worse, localised pain
Motor weakness: paralysis if severe
Sensory changes: less common, clinically useful
Bladder and bowel dysfunction: urinary retention and outflow incontinence
132
Give 4 common sources of mets in the spinal cord
Breast
Myeloma
Nasopharynx
Prostate
133
How would you diagnose spinal cord compression?
MRI
| CT with contrast (can't see spinal oedema/ lesions well)
134
How would you manage spinal cord compression?
Steroids to reduce inflammation e.g prednisolone
| +/- surgery/ radiotherapy
135
Describe and explain the symptoms of cauda equina syndrome
Compression of the cauda equina nerves, usually disc herniation from above
This can cause bladder/ bowel dysfunction
+ saddle/ perianal numbness
+ severe paralysis down the legs/ tingling and numbness
136
How would you manage cauda equina syndrome?
Laminectomy
137
How can you differentiate cauda equina syndrome from sciatica?
Sciatica doesn't cause bladder and bowel dysfunction
138
Give the 4 types of sensory fibres affected in peripheral neuropathies and the associated symptoms
A-alpha: loss of proprioception, sensory ataxia
A-beta: loss of light touch, pressure and vibration sensations
A-delta: myelinated- pain and cold temp (loss of)
C fibres: unmyelinated- pain and warm temp (loss of)
139
Give 5 motor symptoms of peripheral neuropathy
```
Muscle cramps
Weakness
Fasciculations
Atrophy
High arches
```
140
Describe the 3 clinical phenotypes of peripheral neuropathy
Symmetrical sensory motor: longest fibres, hands and feet, initially sensory
Asymmetrical sensory: uncommon, patchy distribution of symptoms, dorsal route ganglia affected (sensory ganglionopathy)
Asymmetrical sensory motor: mononeuritis multiplex
141
How would you diagnose peripheral neuropathy?
Clinical exam: reduced tendon reflexes, sensory deficits, muscle atrophy/ weakness
Neurophysiological exams: nerve stimulation- how well it transmits to determine whether it's demyelinating or axonal damage
(Demyelination: reduced conduction, axonal: reduced amplitude)
142
Give 6 systemic diseases associated with axonal damage
```
Diabetes
Vit D deficiency
Coeliac
Excess alcohol
CKD
Hypothyroidism
Connective tissue diseases
Amyloidosis
```
143
Give 5 Inflammatory/ immune conditions associated with axonal damage
HIV
Hepatitis
Lyme disease
Vasculitis
144
Give two immune mediated conditions associated with demyelination
Chronic inflammatory demyelinating PN
| Multifactorial motor neuropathy
145
Give a genetic cause of demyelination
Charcot-Marie-Tooth disease
146
Describe Gullian-Barre syndrome
Acute neuropathy
Demyelinating/ axonal motor/ sensory motor
Rapidly ascending paralysis and sensory defects
Caused by infection elsewhere/ autoimmune
147
How would you manage peripheral neuropathy?
Treat underlying cause/ symptoms
Balance: physio
Cramps: quinine
Pain: amitryptaline, gaba-pentin, gaba-bal
148
How would you manage Gullian Barre syndrome?
IVIg, plasma exchange (plasmapheresis)
149
Which nerve is affected in Bell's palsy and what are the associated symptoms?
```
Facial nerve (VII)
Symptoms:
Flattening of the forehead
Sagging of the eyebrow
Difficulty closing the eye and mouth (ipsilaterally)
Problems with feeding/ speech
```
150
Give 6 causes of oculomotor nerve palsy (III)
```
Autoimmune: myasthenia gravis
Complication of surgery
Vascular disorders
Tumours/ lesions
Inflammation/ infection
Trauma
Demyelinating disease (MS)
```
151
How might the eye be affected in oculomotor nerve palsy?
Affected eye pupil rolls down and out (inferio-laterally)
Ptosis (drooping of eyelid)
Mydriasis (pupil dilation)
Limitations of eye movement, unable to maintain normal alignment can cause diplopia
152
Describe typical trigeminal neuralgia
Episodes of severe, sudden, shock-like pain in one side of the fat that lasts for seconds-a few minutes
Episodes may be triggered by any touch to the face
153
Give 5 causes of trigeminal neuralgia
```
Loss of myelin around trigeminal nerve due to:
Compression from a blood vessel
MS
Stroke
Trauma
Tumour
Arteriovenous malformation
```
154
How would you treat trigeminal neuralgia?
Carbamazepine (anti-convulsant)
Gabapentin (treat neuropathic pain)
Amitriptyline
Baclofen (to treat spasticity)
155
Describe Brown-Sequard syndrome
Hemiparaplegia
| Hemianaesthesia (on contralateral side)
156
Describe anterior cord syndrome
Below injury level, motor paralysis and loss of pain/ temp
| Proprioception, touch and vibration preserved
157
Describe posterior cord syndrome
Motor function preserved
| Loss of pressure, stretch and proprioception
158
Describe central cord syndrome
Results from cervical spine injury
Greater motor loss in upper body compared to lower
Variable sensory loss
159
Describe carpal tunnel syndrome
Compression of the median nerve causing pain, numbness and tingling, usually due to inflammation of nearby tendons and tissues
160
Describe the components of the carpal tunnel
Bony carpal arch: posterior, floor of carpal tunnel
Flexor retinaculum: Palmar side, roof of carpal tunnel
Running through: flexor tendons for fingers and thumbs, median nerve
161
Describe the symptoms of carpal tunnel syndrome
Initially dull ache/ discomfort
Eventually pins and needles, sharp pain/ parasthesia can extend up forearm
Muscle weakness
Thenar muscle wastage
162
Why is there no loss of central palmar sensation in carpal tunnel syndrome?
Palmar branch is unaffected
163
Give 3 risk factors for carpal tunnel syndrome
Obesity
Pregnancy
Underlying conditions (rheumatoid arthritis)
164
How would you diagnose carpal tunnel syndrome?
Electrophysiological testing
Description of symptoms
Physical tests
165
What is Tinel's sign for carpal tunnel syndrome?
Tapping median nerve, symptoms of tingling/ pins and needles
166
What is Phalen's manoeuvre for carpal tunnel syndrome?
Flex wrists for 1 min, numbness in innervated areas
167
What is Durkan's test for carpal tunnel syndrome?
Manually compress transverse carpal ligament for 30s
| Symptoms arise
168
How would you treat carpal tunnel syndrome?
```
Behaviour modification
Physical therapy
Splinting
Corticosteroids
Surgical division of the transverse carpal ligament
```
169
Describe myasthenia gravis
Autoimmune disease affecting skeletal muscle, patients often wake up feeling fine but weak by the end of the day
170
Which groups are preferentially affected by myasthenia gravis?
Young women 20-30s
| Older men 60s-70s
171
Describe the pathology of myasthenia gravis
B-cells produce antibodies which bind to nicotinic acetylcholine receptor on muscle cell membrane, preventing acetylcholine binding
Antibodies also activate the classical compliment pathway causing inflammation and muscle cell destruction
B-cells also produce muscle specific receptor tyrosine kinase antibodies which target proteins in muscle cells
172
How can myasthenia gravis present as paraneoplastic syndrome?
Underlying cancer
Bronchogenic carcinoma/ thyme neoplasm
Causes a B-cell autoimmune response
173
What is a myasthenic crisis?
Decrease in function of muscles controlling breathing
174
How would you treat myasthenia gravis?
```
Acetylcholinesterase inhibitors (neostigmine/ pyridostigmine): stops Ach breakdown
Immunosuppressive drugs: prednisone (reduce production of autoantibodies
Surgical removal of the thymus: reduces muscle weakness
```
175
Describe the mutation that causes Huntington's disease
Autosomal dominant
| Huntingtin (HTT): chromosome 4 contains a triplet repeat
176
How many repeat and of which sequence would usually cause Huntington's?
>36 CAG repeats (which codes for amino acid glutamine)
177
How does the mutated Huntingtin protein cause symptoms of Huntington's?
Mutated protein builds up in the putamen and caudate of the basal ganglia, causing cell death (excitotoxicity) this causes excessive signalling and an increase in intracellular Ca2+
178
Describe what is meant by anticipation in the context of Huntington's
Due to divisions, child can inherit more CAG repeats than the parents had
More repeats often means earlier onset
179
How does the parent affected change the likelihood of anticipation in Huntington's?
Repeated expansion happens more with sperm production than egg
Anticipation and new disease alleles are more likely to happen if the father is affected
180
Describe the symptoms of Huntington's disease
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Movement problems:
Chorea: dance-like/ jerking movements
Athetosis: slow movements
Abnormal eye movements
Poor co-ordination
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Psychological problems:
Dementia
Personality changes
Depression
181
What is the result of dorsal striatum neuronal death in Huntington's?
Loss of brain tissue and expansion of lateral ventricles
182
What is the typical age of onset of Huntington's?
40 y/o
183
What is the effect on neurotransmitter levels in Huntington's?
Loss of GABA
Loss of acetylcholine
Increased levels of dopamine
184
How might you treat chorea as a symptom of Huntington's?
Neuroleptics: dopamine receptor antagonists
Tetrabenazine: depletes dopamine
