0
Q
How do you test CNII?
A
To test the optic nerve;
Visual acuity (test each eye individually using the best corrected vision)
Visual fields: test all four quadrants of each eye individually ensuring hands are equidistant between examiner and examinee
Pupil: direct and consensual pupillary reflex (afferent limb), accommodation, swinging flashlight test.
Fundoscopy: optic disc oedema, optic disc pallor, venous pulsations, haemorrhages,
1
Q
What sort of things do you inspect in a general neurological exam and mental status examination?
A
Vitals (pulse, BP, temperature) Meningismus, head injury/bruises, battles sign, raccoon eyes, tongue biting CVS: carotid bruins, heart murmurs Mental status: LOC, AVPU, GCS (out of 15) MMSE (out of 30) MoCA Frontal lobe testing for perseveration Clock drawing Orientation to time person and place
2
Q
What are the causes of rapid onset of bilateral blindness?
A
Bilateral occipital lobe infarction, bilateral occipital lobe trauma, bilateral optic nerve damage (as with methyl alcohol poisoning), hysteria.
3
Q
What are the causes of sudden blindness in one eye?
A
Retinal artery occlusion, retinal vein occlusion, temporal arteritis, optic neuritis, migraine, non arteritis ischeamic optic neuropathy.
4
Q
What causes bilateral blindness of gradual onset?
A
Cateracts, acute glaucoma, macular degeneration, diabetic retinopathy (vitreous haemorrhages), bilateral optic nerve damage
5
Q
What controls the parasympathetic supply to the pupils?
A
Parasympathetic supply to the pupils is supplied by the Edinger Westphal nucleus of the third cranial nerve. Stimulation of these fibres causes miosis (constriction of the pupil)
6
Q
What supplies the sympathetic stimulation of the pupils?
A
Fibres from the hypothalamus go to the cilia spinal centre in the spinal cord at C8, T1, and T2 and synapse. Second order neurones exit via the anterior ramus in the thoracic trunk and synapse in the superior cervical ganglion in the neck. Third order neurones travel from here with the internal carotid artery to the eye. Stimulation of the sympathetic fibres causes myadriasis (dilation of the pupils).
7
Q
What controls the efferent path of the pupillary reflexes?
A
Efferent motor fibres from the occulomotor nucleus travel in the wall of the cavernous sinus, alongside the trochlear, abducens and V1 CNs. All of these nerves exit together through the superior orbital fissure. The irisoconstrictor fibres terminate in the ciliary ganglion, where the post ganglionic fibres arise to enervate the iris.
8
Q
What are the different functions of the occulomotor nerve?
A
Sympathetic supply and parasympathetic supply to the iris (sphincter papillae)
Enervates elevator palpebrae superioris (opening of the eyelid)
Controls superior rectus, inferior rectus, medial rectus, and inferior oblique
9
Q
What muscle, and what cranial nerve, is responsible for elevating the eye when adducted?
A
Inferior oblique CN3
Check me
10
Q
Whilst adducted, which CN and muscles elevate and depress the eye?
A
Whilst adducted, the inferior oblique (CN3) elevates the eye, and the superior oblique (CN4) depresses it.
11
Q
What muscles and cranial nerve is responsible for lateral movement of the eye?
A
Lateral rectus (CN6)
12
Q
What muscle and nerve is responsible for the medial horizontal movement of the eye?
A
Medial rectus (CN3)
13
Q
What are the features of a third nerve lesion?
A
Complete potsis (with a complete lesion) Divergent strabismus (eye is 'down and out') Dilated pupil which is in reactive to light (but the consensual reaction in the opposite eye is intact) Unreactive to accommodation
14
Q
What are the causes of a third nerve palsy?
A
Generally caused by trauma or idiopathic.
Central causes include vascular lesions in the brainstem, tumours, and rarely demyelination.
Peripheral causes include: compressive lesions (such as an aneurysm of the posterior communicating artery), tumour, basal meningitis, nasopharyngeal carcinoma or orbital lesions)
Also ischeamia, or infarction as in arteritis, diabetes mellitus, and migraine.
15
Q
What are the features of a fourth nerve lesion?
A
Patient cannot look in and down (think walking down stairs).
Patient may walk with a head tilt.
An isolated fourth nerve palsy is rare and is usually idiopathic or related to trauma. It may occasionally occur due to lesions of the cerebral peduncles.
16
Q
What are the features of a sixth nerve palsy?
A
Failure of the lateral movement, convergent strabismus, and Diplopia. These signs are maximal upon looking to the affected side, and the images are horizontal and parallel to each other.
17
Q
What are the causes of a sixth nerve palsy?
A
Mono neuritis multiplex, and raised intracranial pressure.
Bilateral sixth nerve palsys are caused by trauma or wernicke’s encephalopathy
Unilateral lesions are commonly idiopathic or related to trauma. They may have a central (eg vascular lesion or tumour), or peripheral (raised ICP or diabetes mellitus) origin.
18
Q
What is intern unclear opthalmaplegia?
A
Inter nuclear opthalmaplegia occurs when the is loss of adduction in one eye and there is nystagmus is the abducting eye, it occurs as a result of a lesion in the medial longitudinal fasiculus. This can be caused by MS or vascular disease.
19
Q
What are the causes of horizontal nystagmus?
A
Horizontal nystagmus is caused by a vestibular lesion, or a cerebellar lesion.
20
Q
What causes vertical nystagmus?
A
Vertical nystagmus is caused by brainstem lesions.
21
Q
What can cause of loss of pain and temperature sensation of the face, but not of touch and proprioception?
A
This is caused by lesions of the medulla or upper spinal cord.
22
Q
How do you test the trigeminal nerve?
A
Test the corneal reflex (note, this also tests CN7 and orbicularis occuli)
Test pain and touch.
Inspect for temporal and massater wasting
Test the massater strength
Test the jaw jerk/massater reflex
23
Q
What are the symptoms of a seventh nerve palsy?
A
Difficulty with speaking or keeping fluids in the mouth
Facial asymmetry
Dry eyes or dry mouth (provides stimulus to the lacrimal, sublingual and submandibular glands)
Hyperacusis (paralysis of the stapedius muscle)
The seventh cranial nerve also provides taste for the anterior 2/3 s of the tongue.
24
How do you inspect the seventh cranial nerve?
Check for facial asymmetry,
Test for muscle power (ask patient to look up looking for muscle wrinkling, push against corrugation for strength).
Ask patient to puff out cheeks
Shut eyes tightly (check for bells phenomenon to make sure that they really are trying. Eye goes up)
Ask patient to grin.
If a lower motor neuron lesion is present check the ear and palate for vesicles of herpes zoster (Ramsay hunt syndrome)
25
What causes bilateral facial weakness?
Guillain barre, sarc lidos is, bilateral parotid disease, Lyme disease,or mono neuritis multiplex.
Myopathy and myasenia gravis can cause bilateral facial weakness.
26
How do you test CN12?
Cranial nerve twelve is the hypoglossal nerve. Check for tongue muscle bulk, fasiculations, and strength.
27
How do you test cranial nerve eleven?
Test cranial nerve eleven (the acessory spinal nerve) by testing trapezius and sternocleidomastd strength.
28
How do you test cranial nerves nine and ten?
Cranial nerves nine and ten are the glossy pharyngeal and vagus nerves.
To test these check palatal elevation, gag reflex, vocal cord function, swallowing, taste of the posterior third of the tongue.
29
How do you examine the eight cranial nerve?
Vestibulococlear disease
Check for tenderness of the pinna. Feel for pre and post auricular nodes. Use otoscope to inspect the ear drum.
Test hearing in each ear: finger rubbing/ whispering numbers
Rinnes test: mastoid process and external meats. Rhine positive is when air conduction is better, this is a positive test (normal or sensorineural deafness)
Webers test: put tuning fork in middle of head. A patient with conduction deafness finds the sound louder in the abnormal ear, nerve conduction deafness sound is heard in the normal ear.
Vestibular tests: hall pike manoeuvre to test for benign paroxysmal positioning vertigo.
30
What is the MRC muscle strength scale?
5- full power
4- submaximal power against resistance (can be 4+, 4, or 4-)
3- full range of movement against gravity without resistance
2- full range of movement with gravity removed
1- muscle flicker
0- no muscle contraction
31
Describe the characteristic on examination of a lower motor neuron deficit?
```
Muscle tone is flaccid.
There are some fasiculations
Reflexes are decreased
Down going (flexor) Plantar reflex
Weakness is present.
```
32
Describe the characteristics of an upper motor neurone lesion?
```
Tone is spastic.
No involuntary movements.
Increased reflexes
Up going (extensor) reflex
Weakness is present.
```
33
Describe the characteristics of an extra pyramidal motor deficit.
```
Muscle tone is rigid.
Involuntary movements are present (eg tremor)
Reflexes are normal
Down going plantar reflex
Absent weakness
```
34
What is the nerve root of the biceps reflex?
C5/6
35
What is the nerve root or the brachioradialis reflex?
C6
36
What is the nerve root of the triceps reflex?
C7 is the nerve root of the triceps reflex
37
What is the nerve root of the knee jerk reflex?
L2/L3/L4
38
What is the scoring system for deep tendon reflexes?
```
0 - absent
1 - depressed
2 - normal
3 - increased
4 - Clonus (>4 beats)
```
39
What are the two categories of sensation and how do you test for them?
Spinothalamic tract: pain and temperature
| Dorsal column tract: proprioception and vibration
40
What is the discriminatory touch pathway?
The discriminatory touch pathway is found in the dorsal columns.
The sensory nerve detects sensory information and travels up either the fasiculus cuneatus (T6 and above) or the fasiculus gracilus (Below T6). These neurones synapse in the cuneate and gracile nucleus. The second neuron then crosses via the internal arcuate fibres and goes up the medial lemniscus. It then synapses in the VP thalamus, and connects to the sensory cortex.
41
Describe the spinothalamic pathway.
The spinothalamic pathway carries information regarding pain and temperature from the body.
The first order neuron synapses within 1-2 spinal levels of their entry. The second order neurones then decussate at the level of the synapse. The second order neurones the ascend up the spinothalamic tract, up the spinal lemniscus, and synapse in the VP thalamus.
42
Describe the cortico spinal motor pathway.
Signal starts in the upper motor neurones in the upper motor cortex. This then travels via the internal capsule, through the pyramids, and decussates at the level of the pyramidal decussation in the medulla, and continues to travel down the lateral cortico spinal tract. The upper motor neuron then synapses in the spinal cord at the level that the lower motor neuron leaves and enervates the body.
43
What are the diagnostic uses of a lumbar puncture?
A lumbar puncture is diagnostic for CNS infections (meningitis, encephalitis), inflammatory disorders (MS, guillame barre, vasculitis), subarachnoid heamorrhage (if CT negative), CNS neoplasm (neoplasticism meningitis)
44
What conditions may a lumbar puncture be therapeutic for?
A lumber puncture may be therapeutic for:
Administering anaesthesia, chemotherapy, contrast media,
or for decreasing intracranial pressure in pseudo tumour cerebri or normal pressure hydrocephalus.
45
What are the contraindications of a lumbar puncture?
Raised intracranial pressure (from a mass lesion) that may lead to cerebral hernia ton.
Infection of skin over the wound site
Low platelets or treatment with anticoagulation
Uncooperative patient
46
What's the difference between an upper motor facial lesion and a lower motor facial lesion?
What is the difference between a facial nerve upper motor neuron lesion and a lower motor neuron lesion?
47
What are the opthalmalogical causes of acute vision loss?
Acute angle closure glaucoma, vitreous heamorrhage, retinal detachment, uveitis, trauma.
Endophthalmitis
48
What are the causes of acute loss so vision associated with the optic nerve?
Optic neuritis, anterior ischeamic optic neuropathy (arteritic and non arteritic), compression by space occupying lesions (aneurysm)
49
What are the vascular causes of an acute loss of vision?
TIA/amorosis fugax, central retinal artery or vein occlusion, carotid cavernous sinus fistula
50
What are the different causes of horner's syndrome?
Horner's syndrome is caused by a sympathetic defect that occurs along the path to the head, eye, and neck. Lesions can occur anywhere along the sympathetic pathway on the affected side.
1st order neuron (central): hypothalamus, medulla (lateral medulla stroke= Wallenberg syndrome), spinal tumours, MS, intracranial tumours, syringomyelia.
2nd order neuron (preganglionic): pancoast tumour, paravetebral mass, Carotid artery dissection.
3rd Order neuron (post ganglionic): cluster headache, cavernous sinus mass, trauma, carotid artery dissection
51
What are the common symptoms seen in vitamin B12 deficiency?
Common symptoms seen in vitamin B12 deficiency include: sob, pallor, ,acrobatic aneamia, fatigue, chest pain. Palpitations.
Confusion, or change in mental status
Decreased sense of vibration
Distal numbness and parathesia
Weakness and UMM findings, diarrhoea, and anorexia
52
What are the common causes of dementia?
Primary degenerative: Alzheimer's disease, dementia with Lewy bodies, frontotemporal dementia (Picks disease), Huntingdon's disease, multi-infarct dementia, CNS vasculitis.
53
What are the differential diagnoses for dementia?
(VITAMIN D VEST) Vitamin deficiency (folate, B12, thiamine/B1), Intracranial tumour, Trauma, Anoxia, Metabolic(diabetes), Infection (post encephalitis, HIV), Normal pressure hydrocephalus, degenerative (Alzheimer's, Lewy body, frontotemporal, Huntingdon's, multi infarct dementia, CNS vasculitis).
Vascular, Endocrine (hypothyroid), space occupying lesion (chronic subdural heamatoma), Toxic (alcohol)
54
What is the definition of Alzheimer's?
Alzheimers is progressive cognitive decline interfering with social and occupational functioning characterised by the following:
- anterograde amnesia (impaired ability to learn new memories)
- one of the following cognitive disturbances (aphasia, apraxia, agnosia, disturbance in executive functioning)
55
What types of genetic mutations may lead to Alzheimer's?
Presenillin 1, Presenillin 2, Amyloid precursor protein, E4 polymorphism of apoliprotein E.
56
What is the pathology that is seen in alzeimers?
There is widespread cortical atrophy, especially in the frontal, pareital, and temporal lobes.
Microscopic pathology includes senile plaques (extra cellular deposits of amyloid in the grey matter), neurofibrillary tangles (intra cytoplasmic paired helical filaments with B-amyloid and hyperphosphorylated Tau protein)
Loss of cholinergic neurones in the nucleus basal is of Meynert that project into the frontal cortex.
57
What is dementia with Lewy bodies?
Dementia with Lewy bodies is a progressive cognitive decline interfering with social or occupational function: memory loss may or may not be an early feature. Features of Lewy body dementia include fluctuating cognition with pronounced variation in attention and alertness, recurrent visual hallucinations and Parkinsonism.
Suggestive or supportive features also include REM sleep disorder, sensitivity to neuroleptic medications (develop rigidity, neuroleptic malignancy syndrome, extrapyramidal symptoms), repeated falls.
58
What are Lewy bodies made from?
Lewy bodies are eosinophilic cytoplasmic inclusions. They are found in both cortical and subcortical areas.
59
How do you treat dementia with Lewy bodies?
Treat with acetylcholinesterase inhibitors
60
What is frontotemporal dementia?
frontotemporal dementia is a progressive dementia. It is the third most common cause of cortical dementia (1st = alzeimers, 2nd = DLB), . There are two variants of frontotemporal dementia. The more common variant is the behavioural variant. This is when the patient predominantly presents with social conduct disorder. The second variant, is known as progressive non fluent aphasia and predominantly presents with a disorder of expressive language.
61
What is Creutzfeldt-Jakob disease?
Creutzfeldt-Jakob disease is a rare degenerative fatal brain disorder. CKD is caused by prion proteins causing alterations in the brain such as spongiform changes, astrocytosis, and neuronal loss.
62
Where is Broca's area located? Damage to this area causes what type of aphasia?
Broca's area is located in the posterior inferior frontal lobe. It produces expressive/non fluent aphasia.
63
Where is wernicke's area? Damage to wernicke's area produces what type of aphasia?
Wernicke's area is located in the posterior superior temporal lobe. It is involved with comprehension of language (receptive). Damage to wernicke's area produces fluent aphasia.
64
What are the hallmarks of concussion?
Concussion is mild traumatic brain injury. It is a traumatically induced alteration in mental status that may involve loss of consciousness. Hallmarks include confusion and amnesia that may occur immediately after the trauma or minutes later. Loss of consciousness, if present, must be less than 30 mins, initial GCS must be between 13-15 and post traumatic grade amnesia must be less than 24hours. May also result in impulsivity, irritability, and depression.
65
What provides the main input to the basal ganglia?
The striatum (caudate and putamen) is the input of the basal ganglia . It receives input from the cortex and thalamus to inhibit the globes pallidus pars interna and substantia nigra reticularis promoting movement.
66
What should you consider testing in a young patient <45 yrs who presents with a movement disorder?
In a young patient, consider the need for testing TSH (thyroid disease), ceruloplasmin (Wilson's disease), and CT/MRI (cerebellar disease) as indicated by the type of tremor.
67
What are the three different types of tremor?
The three different types of tremor include postural, intention and resting.
68
What are the causes of a resting tremor?
Parkinsonism, Wilson's disease, mercury poisoning.
69
What are the causes of an intention tremor?
A resting tremor is caused by an intention tremor is caused by brainstem lesions, cerebellar lesions, alcohol, anticonvulsants, sedatives, Wilson's disease.
70
What are the causes of a postural tremor?
The causes of a postural tremor include:
- physiological, anxiety. Essential tremor
- sedatives, drug/EtOH withdrawal, drug toxicity, heavy metal poisoning, CO poisoning,
- thyrotoxicosis, Wilson's disease
- cerebellar
71
What is chorea and what are the differential diagnoses for it?
Chorea are brief abrupt irregular movements. May appear purposeful on milder forms.
Chorea is caused by Huntingdon's disease, neuroacanthosis, SLE, APLA syndrome, Wilson's disease, cerebrovascular disease, tar dive dyskinesia, senile chorea, Sydnams chorea, pregnancy chorea
72
What are the key features of Parkinson's?
TRAP
| Tremor, rigidity, akinesia,/bradykinesia, postural instability.
73
What are the different causes of Parkinson's?
Parkinson's is generally sporadic, caused by a combination of oxidative stress to dopaminergic neurones, environmental toxins, accelerated ageing and genetics. 10% of cases are genetic from alpha synuclein mutations, autosomal recessive Parkin gene or the DJ-1 gene mutation. Rarely caused by MPTP.
74
Describe the pathophysiology of Parkinson's disease.
In Parkinson's disease, there is a loss of the dopaminergic neurones in the pars compacts of the substantia nigra, leading to reduced dopamine levels in the striatum. This means that the is disinhibition of the indirect pathway,and decreased activation of the direct pathway causing increased inhibition of the cortical motor areas.
Alpha synuclein can accumulate in Lewy bodies and cause neuritis in the substantia nigra.
75
How do you treat Parkinson's?
Pharmacologic: levodopa/ carvidopa. Adjuncts/early treatment may also include dopamine agonists, amantadine, MAOI, and anticholinergics.
There are some surgical therapies available. Also treat psychiatric symptoms as needed.
76
What is carbidopa and levodopa?
Levodopa is a dopamine precursor. Carbidopa decreases peripheral metabolism of levodopa, decreasing side effects and increasing the half life of levodopa.
The major complication of levodopa is dyskinesia. There is also levodopa related fluctuation consisting of delayed onset of response, end of dose deterioration, often referred to as 'on' and 'off' time.
77
What type of gait does cerebellar ataxia produce?
Wide based gait without high stepping, veers to the side of the lesion due to cerebellar lesion.
78
What is the cause of Huntingdon's disease?
Huntingdon's disease is caused by autosomal dominant CAG repeats on chromosome 4 (with anticipation) in the Huntingdon gene on chromosome 4. The CAG repeats leads to the accumulation of a defective protein in neurons. This leads to global cerebral atrophy, especially affecting the striatum, that leads to increased activity of the direct pathway and decreased activity of the indirect pathway.
79
What are the signs and symptoms of Huntingdon's chorea?
Huntingdon's chorea typically presents at 35-44 yrs but varies with anticipation. It typically presents with clumsiness, fidgeting, and irritability. This then progresses over the years to frank dementia, psychosis, and chorea. The chorea beings as a movement of the eyebrows and forehead, shrugging of the shoulders, and parakinesia (pseudo purposeful movement to mask involuntary limb jerking). Progresses to dance-like or ballism, and in the late stage is replaced by dystopia and rigidity. They experience dementia, mood changes, and psychosis. MRI shows enlarged ventricles and atrophy or the cerebral cortex.
80
How does botulinum toxin work?
Botulinum toxin acts by preventing the release of ACh at the neuromuscular junction.
81
How do you treat tic disorders?
Dopamine blocker
82
What happens if there is degeneration of the vermis?
There is trunk/gait ataxia
83
What happens if there is degeneration of the cerebellar lobe?
Rebound phenomenon, scanning dysarthria, dysdiadochokinesis, dysmetria, nystagmus.
84
What are the signs and symptoms of cerebellar dysfunction?
Nystagmus, dysarthria, ataxia, dysmetria, dysdiadochokinesis, postural instability, intention tremor, hypotonia, pendulum patellar reflex, rebound phenomenon, gaze apraxia.
85
What is wernicke Korsakoff's syndrome?
Wernicke Korsakoff syndrome is a deficiency of thiamine due to alcohol abuse.it causes apathy, confusion, impaired extra ocular movements, ataxia (truncal and gait), without treatment it progresses to encephalopathy and untimely death. Treat with thiamine with glucose.
Korsakoff's syndrome is a progressive decline of both anterograde and retrograde memory that cannot be reversed by thiamine. Note that alcohol can also cause a cerebellar ataxia seperate from thiamine deficiency.
86
What kind of gait does sensory ataxia produce?
Sensory ataxia produces a wide based with high stepping and positive Rohmbergs due to loss of positional sense.
87
What is amyotrophic lateral sclerosis?
ALS is the most common type of motor neuron disease. It causes a progressive degeneration and loss of motor neurons with astrocytic gliosis that results in the production of both upper motor neuron and lower motor neuron symptoms.
88
What are the signs and symptoms of ALS?
Onset generally between the ages of 40-60
Limb motor symptoms: segmental and asymmetrical UMN and LMN signs.
Bulbar findings: dysarthria, dysphagia, tongue atrophy, and fasciculations
Pseudobulbar affect or emotional lability
Sparing of occular muscles and sphincters.
It is NOT ALS if there are: sensory symptoms, predominant pain, bowel or bladder incompetence, cognitive impairment, ocular muscle weakness.
89
What investigations and findings are made for ALS?
EMG shows denervation, reinnervation, fasciculations.
Muscle biopsy shows small angulated fibres from denervations.
Rule out cord disease/compression with CT or MRI and peripheral neuropathy with NCS
90
Apart from ALS, what are the other motor neuron diseases?
Progressive muscular atrophy/bulbar palsy (only LMN symptoms with asymmetric muscle weakness)
Primary Lateral Sclerosis(progressive pseudobulbar palsy): UMN symptoms, later onset, not fatal with variable disability.
Spinal muscular atrophy: peadiatric disease with symmetric LMN symptoms
Post polio syndrome: residual asymmetric muscle weakness, atrophy
Multifocal motor neuropathy: conduction block on NCS, asymmetric LMN symptoms
91
What is Tinel's sign and Phalen's Test?
Tinel's Sign involves tapping over the median nerve at the wrist to elicit symptoms of carpal tunnel
Phalen's Test involves holding both wrists in forced flexion (with dorsal surfaces of the hands pressed together) for 30-60 seconds. Test is positive is symptoms of carpal tunnel are elicited.
92
What is a monoradilculopathy? What causes it?
A monoradiculopathy is a single dermatonal deficit due to a single nerve root lesion. Monoradiculopathies are caused by disc herniations or root compression. There generally isn't much tactile anaesthesia as dermatomes tend to overlap.
93
What is a polyradiculopathy?
Polyradiculopathies are multiple dermatonal deficits due to multiple nerve root lesions. A well known example of a polyradiculopathy is cauda equine syndrome that affects the lumbrosacral roots.
94
What is a plexopathy?
A plexopathy is a deficit matching the distribution of a nerve plexus. there is a brachial plexopathy. Upper brachial plexopathy affects C5-C7 (Erb's palsy) resulting in LMN symptoms of shoulder and upper arm muscles. Lower brachial plexopathy affects C8-T1 (klumpke's palsy) affecting LMN sx and sensory Sx or the hand and forearm.
Caused by trauma, idiopathic neuritis, tumour infiltration, radiation, thoracic outlet syndrome (cervical rib).
95
What is carpal tunnel syndrome?
Carpal Tunnel Syndrome is the most common type of polyneuropathy. It occurs due to compression of the median nerve at the wrist. Symptoms include wrist pain, and parathesia of the first 3 1/2 digits, worse at night.
Exam: Tinel's Sign, Phalen's sign, sensory deficit, thenar muscle wasting, weakness of thumb abduction (abductor pollucis brevis)
EMG and NCS show slowing at the wrist.
96
What are the different neuropathies seen in diabetes?
- Peripheral Neuropathies: Pain or loss of sensation in a glove and stocking distribution (hands and feet affected before arms and legs)
- Autonomic: anhydrosis, orthostatic hypotension, impotence, gastroporesis, bowel and bladder dysfunction.
- Mononeuropathy multiplex: nerve infarct or compression
- Cranial neuropathy
- Lumbrosacral plexopathy
97
What are the causes of carpal tunnel?
- Idiopathic
- Pregnancy
- Heart Failure/Oedema
- Rheumatoid arthritis
- Lunate fracture
98
How do you treat carpal tunnel?
Corticosteroid injections
Wrist splint
Surgery (flexor retinaculum division)
99
What is Guillame Barre Syndrome?
Guillame Barre syndrome in an autoimmune demyelinating polyneuropathy that affects all four limbs, generally affecting the lower limbs before the upper limbs. It generally occurs following an infection (typically campylobacter jejuni). Patient presents with motor weakness (affecting proximal before distal), back pain, reduced reflexes and minimal sensory symptoms. there may be cranial nerve involvement and autonomic involvement.
100
What is normal pressure hydrocephalus?
Normal pressure hydrocephalus is a reversible cause of dementia in the elderly. It is thought to be caused by reduced absorption of CSF by the arachnoid villi. these changes may be secondary to head injury, subarachnoid haemorrhage, or meningitis. The classic triad of dementia, gait abnormality (similar to parkinsons) and urinary incontinence is seen. Imaging shows hydrocephalus with an enlarged fourth ventricle. Manage with ventriculoperitoneal shunting.
101
What is tuberous sclerosis?
Tuberous sclerosis is a genetic condition of autosomal dominance that presents with neurocutaneous features.
Cutaneous features: Depigmented 'ash leaf' spots, Shagreen patches (patches of rough skin over spine), adenoma sebaceum (butterfly rash),subungal fbromata, café au lait spots.
Neuro features: epilepsy, intellectual impairment, developmental delay.
Other: retinal hamartomas (dense white areas on retina), Polycystic kidneys, rhabdomyomas of the heart.
102
What is the deficit produced in an anterior cerebral artery stroke?
Contralateral hemiparesis and hemiplegia
| affecting lower limb > upper limb
103
What is the deficit produced by a middle cerebral artery stroke?
- Contralateral hemiparesis and hemiplegia affecting upper > lower limbs.
- Contralateral Homonymous Hemianopia
- Aphasia
104
What is the deficit produced by a posterior cerebral artery stroke?
- Contralateral Homonymous Hemianopia with macula sparing
| - Visual Agnosia
105
What causes Weber's Syndrome? What are its symptoms?
Weber's syndrome is causes by stroke in the branches of the posterior cerebral artery that supply the midbrain. It produces:
- Ipsilateral Occulomotor palsy (CNIII)
- Contralateral hemiparesis
106
What produces Wallenberg Syndrome/Lateral Medullary Syndrome?
Wallenberg Syndrome/ Lateral Medullary syndrome is caused by a stroke affected the Posterior Inferior Cerebellar Artery.
It causes:
-Ipsilateral pain and temperature loss on face
-Contralateral pain and temperature loss on the body
-Ataxia
-Nystagmus
107
What produces Lateral Pontine Medullar Syndrome?
Lateral Pontine Medullary Syndrome is caused by damage to the Anterior Inferior cerebellar artery. It produces a syndrome very similar to Wallenberg's syndrome except there is facial paralysis and deafness.
108
What sort of syndrome does a stroke to the basilar artery produce?
A stroke affecting the basilar artery produces 'Locked-In' syndrome
109
What is amaurosis fugax?
Amaurosis fugax is transient monocular loss of vision caused by ischeamia/haemorrhage in the ophthalmic or retinal artery, often caused by atheroma of the carotid artery.
110
What is the typical presentation of a lacunar stroke?
A lacunar stroke can affect the thalamus, basal ganglia, or the internal capsule. It is often associated with hypertension.
A lacunar stroke can often present with hemiparesis, hemiplegia, or hemiplegia with ataxia.
111
What is syringomyelia? What are its features?
Syringomyelia is the is the development of a cavity in the spinal cord. If it extends into the medulla then it becomes a syringobulbia. Sryringomyelia is strongly associated with Budd-Chiari Malformation.
112
What is erythema nodosum?
Erythema nodosum is inflammation of the subcutaneous fat. It typically causes tender, erythematous, nodular lesions. It usually occurs over the shins, but may occur elsewhere. Normally resolves within six weeks. Lesions heal without scarring.
113
What are the causes of erythema nodosum?
Erythema Nodosum can be caused by:
Infection: TB, stroptococcus, brucellosis
Systemic Disease: malignancy/lymphoma
Drugs: penicillins, sulphonamides,combined oral contraceptive
Pregnancy
114
What are the typical features of an extradural heamatoma?
An extradural heamatoma is also known as an epidural heamatoma (bleeding between the dura mater and the skull). It shows features of raised intracranial pressure and often exhibits a lucid period.
Extradural heamatomas are gnerally caused by excelleration/decelleration accidents, or to trauma to the temporal region (causing a rupture of the middle meningeal artery).
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What are the typical features of a subdural heamatoma?
A subdural heamatoma involves bleeding between the arachnoid layer and the dural layer of the meninges. It most often occurs around the frontal and pareital lobes. Triggers include old age, alcoholism, and anticoagulation. It is often slow in onset and features fluctuating confusion and consciousness.
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Whats the difference between axonal and demyelinating neuropathies of nerve conduction studies?
On NCS, axonal neuropathies have decreased amplitude, demyelinating neuropathies has decreased velocity.
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What is the ddx of demyelinating polyneuropathies?
Guillame Barre Syndrome, Chroninc Inflammatory Demyelinating Polyneuropathy.
Diptheria, amiodarone
Charcot-Marie-Tooth
Storage diseases, pressure palsy predisposition
Paraneoplastic
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What is the typical presentation of a polyneuropathy? What are the most common causes?
Polyneuropathies typically present with a symetrical distal stocking-glove pattern (affecting the longest motor fibres first). Also presents with hypotonia, progression of dysthesia early and weakness later. Caused by diabetes mellitus, renal disease, substances, toxins, or are hereditary. Also caused by SLE, HIV, leprosy, alchol B12 deficiency, ureamia.
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Why is Guillame Barre a neurological emergency?
Guillame Barre is a neurological emergency due to the risk of imminent respiratory failure.
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What are the findings on CSF in Guillame Barre syndrome? What are the findings on NCS and EMG?
Normal White Cell Count, high protein.
| On NCS/EMG there is conduction block, differential or focal slowing (motor>sensory), decreased F wave.
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What is the prognosis for Guillame Barre?
Guillame Barre has a 5% mortality rate.
| There is a peak of symtpoms at 2-3 weeks, with resolution at 4-6 weeks. 7-15% suffer from permanent defects.
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What are the different subtypes of Guillame Barre?
- Acute Inflammatory Demyelinating Polyneuropathy (AIDP)
- Acute Motor Sensory Axonal Neuropathy (AMSAN)
- Acute Motor Axonal Neuropathy (AMAN)
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How do you treat Guillame Barre?
- Admit, moniter vital signs and vital capacity due to risk of respiratory failure, manage dysautonomia, manage pain.
- IVIg and plasmapheresis.
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What are the typical features of Neuromuscular Junction disease? What are the different types of neuromuscular junction diseases?
The most typical feature of neuromuscular junction disease is fatigue. Fatigue can be demonstrated by getting someone to look up or hold their hands out.
The three different types of diseases of the NMJ are: myasthenia gravis, Lambert Eaton syndrome, and Botulism.
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What is the pathophysiology of Myasthenia Gravis?
Myasthenia Gravis is an autoimmune disorder caused by auto-antibodies. Autoantibodies cause damage and blockade of the post synaptic achetylcholine receptors. 15% have thymic neoplasia, and 85% have thymic hyperplasia.
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What is the typical presentation of Myasthenia Gravis?
Myasthenia Gravis typically presents in women in their 20s, or men in their 60s. There is fatiguability and weakness of the skeletal muscles without reflex changes, sensory changes, or coordination abnormalities. Occular symptoms (diplopia, ptosis), bulbar symptoms (dysarthria/dysphagia). It then affects the neck flexors and extensors, and then proximal limb weakness. Respiratory weakness may lead to respiratory failure.
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How do you investigate Myasthenia gravis?
Edrophonium ('Tensilon') Test. Edrophonium is a drug that inhibits Acetylcholinesterase activity, providing immediate releif. Causes respiratory difficulty or bradycardia in a Cholinesterase crisis.
EMG: repetative stimulation shows a decremental response. Single fibre EMG shows a jitter.
Spirometry
Anti-acetylcholine receptor antibody assay.
CT/MRI to screen for thymoma/thymic hyperplasia.
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How do you Myasthenia Gravis?
-Thymectomy (85% of patients show improvement or remission
- Pyridostigmine (acetylcholinesterase inhibitor)
-Immunosuppression: steroids, azathioprine, cyclophosphamide, and mycophenalate
To manage a short term crisis give IVIg and plasmapharesis.
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What is Lambert-Eaton syndrome?
55-60% of cases of Lambert-Eaton Syndrome are associated with small cell carcinoma of the lung. There is downregulation of presynaptic voltage gated calcium channels secondary to specific channel binding antibody, causing decreased amounts of
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