Neurology Flashcards
1
Q
In diplopia, which is the false image?
A
The outermost image is always false. Cover each eye in sequence. When the outermost image disappears, this is the eye with extraoccular muscle weakness.
2
Q
What facies is this?
A
Acromegalic facies
3
Q
Name the syndrome
A
Cushing’s syndrome
4
Q
What facies is this?
A
Myaesthenia snarl - when asked to smile, the snarl is the result of contraction of the middle part of the mouth without contraction of the muscles on the sides of the mouth.
5
Q
What is the facies? What are its features?
A
Frontal balding, bilateral ptosis, bilateral face weakness with thin facial muscles. AKA Hatchet Facies of myotonic dystrophy.
6
Q
Which phase of nystagmus is pathologic?
A
The slow phase that follows the fast phase
7
Q
What does cerebellar nystagmus look like?
A
Unilateral or bilateral. The slow phase drifts back to the centre during horzontal gaze, with the fast phase in the direction of gaze.
8
Q
What are you looking for when you examine a patients head and scalp as part of a cranial nerve exam?
A
Craniotomy scars
Neurofibromata
Cushings syndrome
Acromegaly
Paget’s disease
Facial asymmetry and obvious ptosis
Proptosis
Skew deviation of the eyes
Obvious pupil inequality
Myaesthenia snarl
Myotonic hatchet face
9
Q
What is strabismus?
A
Abdnormal resting alignment of the eyes (aka a ‘squint’)
10
Q
What does peripheral vestibular nystagmus look like?
A
-Unidirectional, normally horizontal but occasionally has torsional element.
-It gets worse when the eyes move in the direction of the fast phase
-It improves when the eyes are allowed to move towards the slow phase.
-Abnormal head impulse test (rapidly, without hurting the pt, move their head and watch for loss of vestibulo-ocular reflex - eyes follow head and corrective saccade occurs)
-Nystagmus can be monocular and occur in the setting of weakness of the other eye.
-
11
Q
What is the significance of vertical nystagmus?
A
Almost exclusively indicates a central disorder
12
Q
What is Alexander’s Law?
A
States that the slow-phase velocity of the nystagmus caused by unilateral vistubular lesion increases with gaze in the beat direction. In other words, the nystagmus gets worse if gaze goes towards nystagmus.
13
Q
What’s the most helpful feature for delineating congential nystagmus from other forms?
A
Patient doesn’t experience the world moving
14
Q
What does multidirectional nystagmus in a gaze-evoked pattern suggest?
A
Generalised cerebeller dysfunction - more commonly caused by drug toxicitiy (e.g. anticonvulsants are a common cause).
15
Q
What is tested by doing a jaw jerk?
A
Testing the reflex arc between cranial nerve 5 sensory components and motor components.
16
Q
What are the three features of pseudobulbar palsy?
A
Dysphagia, dysarthria and emotional apathy.
Other possible features include sialorrhoea, dysphonia (hypernasal), glossoplegia, emotional lability, poverty of facial expression, pathalogical laughter, trismus, frontal release signs, cognitive impairment and seizures.
17
Q
What is pseudobulbar palsy?
A
It’s a a collection of symptoms that results from bilateral corticobulbar tract lesions - upper motor neuron signs impacting the muscles of the face. Also referrerd to as bilateral upper motor neurone IX, X and XII nerve palsy.
18
Q
What is the corticobulbar tract?
A
Fibres from the motor and pre-motor cotrex via the the cranial nerve nuclei that provide motor input to the muscles of the face + the trapezius and SCMs.
19
Q
In a speech exam, what is the reason to do a jaw jerk?
A
If the patient presents with dysarthria without evidence of wasting, then a jaw jerk can be done to test the integrity of the corticobulbar tract. Bilateral corticobulbar tract defects will lead to a brisk jaw jerk. This will help to distinguish upper motor neuron defects (pseudobulbar palsy) from cerebellar disease.
20
Q
What nerves are involved in the corneal reflex?
A
V1 opthalmic sensory branch, and the motor part of the 7th nerve
21
Q
Why test light touch and pain over the 5th nerve regions?
A
A medullary or upper cervical lesion of the fifith nerve causes loss of pain and temperature sensation with preservation of light touch. A pontine lesion may cause loss of light with perservation of pain and temperature sensation.
22
Q
What does a deviated uvular indicate?
A
A unilateral tenth nerve lesion on the side the uvular is pointing away from.
23
Q
Regarding the rule of 4s, what are the four structures in the midline of the brainstem?
A
The midline structures all begin with M.
1. The motor pathway (corticospinal tract)
2. Medial lemniscus (continuation of the dorsal column - vibration, proprioception)
3. The medial longitudinal fasciulus
4. Motor nuclei of the cranial nerves (3, 4, 6 and 12)
24
Q
Regarding the rule os 4s, what the four structures that sit in the lateral parts of the brain stem?
A
The lateral structures all begin with S (Side structures).
1. Spinocerebellar pathways
2. Spinothalamic pathway
3. Sensory nucleus of the 5th nerve.
4. Sympathetic pathway
25
What are the 4 cranial nerves that have nuclei in and above the midbrain?
1 and 2 have nuclei above the brainstem. Occulomotor and trochlear are in the midbrain. Trigeminal kind of extends up into the midbrain a bit as well.
26
What are the 4 cranial nerves that have nuclei in the pons?
Trigeminal, abducens, facial and vestibulocochlear. AKA 5/6/7/8
27
What 4 cranial nerves have nuclei in the medulla?
Glossopharyngeal, vagus, spinal accosory and hypoglossal nerves.
28
What deficits are likely to be found in a medial medullary syndrome?
Using the rule of 4s, the medial structures are:
1. The 'medial leminiscus' (proprioception and vibration) - this will cause contralateral vibration and proprioception loss
2. The medial motor nuclei (at the level of the medullar) - those that divide into 12. So, that leaves just nerve 12. This will lead to ipsilateral weakness of the tongue.
3. Motor pathways: weakness and upper motor neuron signs in the contralateral upper and lower limbs.
Note that they MLF is unaffected as it extends from the Pons to the Midbrain and is not involved in the medullar.
29
What cranial nerve nuclei are located medially in the brainstem?
Those that are 1. in the brainstem and 2. divide evenly into the number "12"
So - cranial nerves 3, 4, 6 and 12 are located medially.
30
What cranial nerve nuclei are located laterally in the brainstem?
Those that do not divide neatly into the number "12".
So - cranial nerves 5, 7, 8, 9, 10, 11
31
What neurological deficits would you expect to find in a lateral medullary syndrome?
All lateral structures per the rule of 4s at the the level of the medullar:
1. Spinocerebellar dysfunction leading to ipsilateral ataxia of the arms and legs.
2. Spinothalamic dysfunction leading to contralateral sharp/dull dysfunction
3. Sympathic pathway involvement leading to an ipsilateral horners syndrome
4. The lateral meduallary CN nuclei may be affected - CN9 deficit will lead to ipsilateral sensation loss of the oropharynx, CN10 deficit will lead to ipsilateral pharyngeal arch weakness, and a CN11 deficit will cause ipsilateral trapezious and sternocleidomastoid weakness.
32
Do cranial nerve nuclei innervate contralateral or ipsilateral structures?
Ipsilateral
33
If you detect a lower 7th facial nerve palsy, what should you do next?
Check in the ear for VZV vesicles of ramsey hunt, look in the mouth fo vesicles also,
34
What are the components of a HINTS exam?
Head impulse, nystagmus, test of skew.
35
What is a normal head impulse test?
Normally, the vestibulo-ocular reflex allows a person to focus on a object whilst the head moves around. This is lost in peripheral vertigo syndromes, with the eyes having to perform a corrective saccade in order to keep focus on the face when quickly moving the head to the left or right.
36
What do tongue fasiculations and wasting indicate?
12th nerve palsy - peripheral
37
What is one-and-a-half syndrome?
Ipsilateral eye horizontal gaze paralysis (cannot adduct or abduct with horizontal gaze). Contralateral eye INO (cannot adduct beyond the midline with gaze). Convergence is normal.
In neutral gaze, the contralateral eye is slightly abducted (paralytic pontine exotropia).
Causes: 1) lesion in the 6th nerve nuclei AND the MLF on the same side OR 2) in the paramedian pontine reticular formation (PPRF - horizontal gaze centre) on the ipsilateral side to the paralysed eye.
38
Explain what goes wrong to cause an internuclear opthalmoplegia (INO).
The horizontal gaze centre at the top of the pons is caused the paramedian pontine reicular formation PPRF. When looking to the right, the PPRF stimulates the ipsilateral abducens nucleus which innervates the lateral rectus of the ipsilateral eye to look in that direction. Simultaneously, the interneurons from stimulated abducens nerve project to form the medial longitudinal fasciulous and synapse with the contralateral third nerve nucleus. This innervates the contralateral medial rectus and causes the contralateral eye to move in the same direction as the ipsilateral eye. Lesions of the medial longitudinal fasciculus interupt the communication to the contralateral eye from the ipsilateral abducens nucleus and so the contralateral eye does not adduct beyond the midline.
39
What is the structural reason that bilateral INOs occur frequently?
Becasue the 2x MLF tracts run very close to each either in the midline of the brainstem from the pons through the midbrain. Runs from the 6th to 3rd nerve nuclei.
40
Why is vergence maintained in an MLF lesion induced INO?
Vergence is coordinated by CNIII nuclei and doesn't rely in the MLF connection between the 6th and 3rd nuclei.
41
What is an 8 and a half syndrome?
One and half syndrome with a lower motor 7th nerve palsy
42
What is the differential for a one and a half syndrome?
MS, stroke
43
Which parts of the 5th cranial nerve nuclei are responsible for sharp dull perception in the face, and which part is responsible for light touch perception?
The 5th nerve spans the pons and the medulla.
Isolated medullary 5th nucleus lesion - loss of pain, preserved light touch senstion of the face.
Isolated Pontine 5th nucleus lesions - loss of light touch, preserved pain sensation on the face.
44
What's a good differential for Horner's syndrome?
Carcinoma of the lung apex (usually SCC)
Neck issues - thyroid malignancy or trauma
Carotid arterial lesions - aneurysms, dissection, pericarotid tumours, cluster headaches
Brain stem lesions - vascular disease (lateral medullary syndrome, syngobulbia tumour)
Retro-orbital lesions
Syringomyelia
45
What should you check in the hands if you detect horners?
Clubbing, interosseus muscle wasting, C8/T1 abduction power
46
What causes an absent light reflex, but a normal accomodation reflex?
Midbrain lesions (neurosyphyllis) - Argyll Robertson pupils
Ciliary ganglion lesion
Parinaud's syndrome
Bilateral anterior visual pathway lesions
47
Where is the PPRF?
The paramedian pontine reticular formation - is in the midline of the pons
48
Where is the rostral interstitial nucleus? What is it?
It's the vertical gaze centre. It's in the MLF.
49
What is the pathway for the accomodation reflex?
Afferent signal via CNII bilaterally to the lateral geniculate nucleus, thalamus, and cortical visual structures of the occipital lobe. Concious control or the reflexive presence of something close to the face leads to bilateral activation of medial recti via the third nerve nuclei, and parasympthetic stimulation of ciliary muscles leads to pupilary miosis via the endiger westphal nucleus.
50
What can cause loss of accomodation reflex but presence of light responsive pupils?
Occipital lobe lesions (cortical blindness) or a midbrain lesion
51
What is Adie's syndrome?
A lesion in the efferent parasympathtic pathway to the ciliary ganglion, or between the ciliary ganglion and the iris. It leads to a dialted pupil that doesn't respond to light or accomodation correctly. Pts often have decreased tendon reflexes. Commonly young woman.
52
What are the causes of an Argyll Robertson pupil?
Pupillary constriction to accomodation but not to light.
1. Syphilis
2. Diabetes mellitus
3. Alcoholic midbrain degeneration
4. Other midbrain disease
53
Where is the edinger westphal nucles located?
In the midbrain
54
What is tabes dorsalis?
Loss of vibration sensation and priprioception associated with neurosyphilis.
55
Clinically what is the difference between papilloedema an papilitis?
Papilitis is painful and swollen and has a greater impact on function. So, compared with with non-painful swelling (papilloedema), papilitis causes reduced visual acutiy, red desaturation, large central scotoma, pain on eye movement. Papilitis is a feature of optic neuritis, and is usually unilateral. Papilloedema is a feature of raised ICP, and is bilateral.
56
Differential for papilloedema?
Space occupying lesion
Hydrocephalus
-obstructive
- communicating
Retroorbital mass
57
Differential for papilloedema?
Space occupying lesion
Hydrocephalus
- obstructive
- communicating
--increased formation or decreased absorption
Retroorbital mass
Idiopathic intracranial hypertension
- idiopathic
- contraceptive pill
- Addison's disease
- Drugs (nitrofurantoin, steroids, tetracycline vit A)
- Lateral sinus thrombosis
- head trauma
Hypertension (grade IV)
Central retinal vein thrombosis
Cerebral venous sinus thrombosis
High cerebrospinal fluid protein level (in e.g. GBS)
58
Causes of optic atrophy?
Chronic papilloedem or optic neuritis
Optic nerve pressure or division
Glaucoma
Ischaemia
Familial - retinitis, Leber's disease, Friedreich's Ataxia
59
What is Friedreich ataxia?
The most common hereditary ataxia, caused by mitochondrial protein (fraxin) triplet repeat (GAA) disease. Age at onset: depends on number of GAA repeats - most common in adolescence. Anticipation. Ataxia in all four limbs, reflexes lost in ~90% of patients, motor weakness involving the feet and legs first, then the arms later. Cerebellar dysarthria. Sensory loss in distal limbs. Dysphagia is common. Pes cavus. Cognition is usually preserved,
60
Causes of optic neuropathy with papillitis?
MS
Toxic - ethambutol, alcohol, nictotine, chloroquine
Metabolic - b12
Iscahaemia - Diabetes mellitus, TA, atheroma
Leber's disease (mitochondiral disease)
Mononucleosis
61
Cataract causes?
Old age
Diabetes mellitus
Steroids
Hereditary and congenital causes
Glaucoma
Irradiation
Trauma
62
Causes of ptosis with normal pupil size?
Senile
Myotonic dystrophy
Fascioscapulohumeral dystrophy
Ocular myopathy
Thyrotoxic myopathy
Myasthenia gravis
Botulism
Snake bite
Congential
Fatigue
63
What are the features of a CNIII palsy?
Complete ptosis
Divergent strabismus (down and out)
Dilated and unreactive pupil
64
How do you check for a CNIV palsy in a patient with a CNIII palsy?
Ask the patient to look down and across the opposite side of the lesion, and look for intorsion. The CNIV innervates the superior oblique which causes intorsion.
65
What cranial nerves are impacted by lesions in the cavernous sinus?
CNII, CNIII, IV, V (occular and maxillary branches), and VI
66
What are the important non-CN structures in the cavernous sinus?
Veins, internal carotid artery, pituitary gland
67
Differential for CNIII opthalmoplegia?
Aneurysms (PICA)
Tumiour causing raised ICP
Nasopharyngeal carcinoma
Orbital lesions
Basal meningitis
CNIII nerve infarction - arteritis, diabetes
Trauma
Cavernous sinus lesions
68
Features of a sixth nerve palsy?
Lateral eye movement failure
Affected eye becomes deviated inwards in severe lesions
Diplopia - maximal when looking at the affected side
69
What are the examination findings found in pseudotumour cerebri?
AKA indiopathic intracranial hypertension or other causes of raised ICP.
Papilloedema
Changes in visual acuity
Enlarged blind spot
Pulsatile tinnitus
Bilateral cranial nerve IV palsy
70
Differentials of a bilateral sixth nerve palsy?
Trauma
Wernicke's encepahlopathy
Raised ICP
Mononeuritis multiplex
71
Differentials for a unilateral sixth nerve palsy?
Central causes
- vascular
- tumour
-Wernicke's encephalopathy
-MS (rare)
Periperhal
- diabetes
- trauma
- idiopathic
- raised ICP
72
What muscle is responible for downward gaze of the eye when it is adducted?
The superior oblique - innervated by the fourth nerve
73
What muscle is responsible for downward gaze when the eye is abducted?
The inferior rectus - innervated by the third nerve
74
What are the causes of jerky horizontal nystagmus?
Vestibular lesions
Cerebellar lesions
INO (in the unaffected side)
75
What are the causes of jerky vertical nystagmus?
Brain stem lesions
- upbeat -> floor of the fourth ventricle
- down beat -> foramen magnum lesion
Toxic
- phenytoin
- alcohol
76
What are the causes of pendular nystagmus?
Retinal (AMD, albinism)
Congenital nystagmus
77
How does supranuclear palsy affect gaze?
Loss of vertical upward and/or downward gaze.
78
How do you differentiate a supranuclear (higher centre) palsy loss of vertical gaze from 'nuclear plasy' (e.g. CNIII or vertal gaze centre lesions)
Dolls head eye movement reflexes in the vertical plane (i.e. able to fixate on an object) throughout neck flexion and extension.
Also, in PSP, both eyes are affected, pupils are often unequal, and there is no diplopia.
79
What are the occular findings in progressive supranuclear palsy (the Parkinson's plus syndrome), as opposed to supranuclear palsy?
Downward gaze is lost first in PSP
--then upward gaze, then horizontal gaze as well
Saccades impaired before pursuit
Associated with pseudobulbar palsy (+jaw jerk), long tract signs, extrapyramidal signs, dementia and a rigid neck.
80
What is parinaud's syndrome?
Loss of vertical upward gaze
Convergence-retraction nystagmus on attempted convergence
Pseudo-argyll robertson pupils (loss of light pupillary reflex, but constriction to near focus)
81
What causes parinaud's syndrome?
Central lesisons impacting the dorsal (tectal) midbrain
- pinealoma
- MS
- vascular lesions
Peripheral
- trauma
- diabetes mellitus
- other vascular lesions
- idiopathic
- raised ICP
82
What does tectum mean in relation to the midbrain?
Tectum is latin for roof. It's the dorsal part of the midbrain.
83
What's the differenetial diagnosis of a 5th nerve palsy?
Central (pons/medullar/upper C spine)
- vascular, tumour, syringobulbia, multiple sclerosis
Peripheral (posterior fossa lesiosn)
-aneurysm, base of skull tumour (e.g. acoustic neuroma), chronic meningitis
Trigeminal ganglion (petrous temporal bone)
- meningioma, fracture of the middle fossa
Cavernous sinus
- tumour, aneurysm, thrombosis
Other
- SLE, Sjorgren's, toxins, idiopathic
84
How to delinate between peripheral or central 5th nerve lesions?
Central lesions typically will impact all 3 territories, but only one modality
- light touch is lost in pontine lesions affectiving the 5th nerve nucleus, but pain is preserved
-pain is lost in lesions that impact the medullar or upper C-spine, but light touch is preserved
In peripheral lesions - both light touch and pain sensation will be lost. If the lesion is in the posterior fossa or at the trigeminal ganglion.
85
What are the upper motor neuron causes of a 7th nerve palsy?
MND, vascular or tumour.
86
What are the lower motor neuron causes of a 7th nerve lesion?
Pontine
- vascular, tumour, syningobulbia or MS
Posterior fossa
- acoustic neuroma or meningioma
Petrous temporal bone
-Bell's palsy
-Ramsay Hunt
-Otitis media
-Fracture
Parotid
-tumour
-sarcoid
87
What can cause bilateral 7th nerve palsy?
GBS
Bilateral parotid disease (e.g. cancer or sarcoidosis)
Mononeuritis multiplex
88
What is Rinne's test?
Tuning fork to the mastoid process behind the ear, then when it can no longer be heard, in front of the meatus of the external auditory canal. If it cannot be heard when its moved, the person has conduction deafness.
89
What is Weber's test?
Place tuning fork on the forehead. Sound is heard in the middle of the forehead -> normal. Abnormal results - sound is louder in an ear with conduction deafness. OR sound is quiter in the ear with nerve deafness.
90
What's the differential diagnosis for a unilateral twelth nerve palsy?
Central
- vascular (vertebral artery thrombus)
- motor neuron disease
- syringobulbia (fluid cavity in the spinal cord that involves the lower brain stem)
Peripheral
-aneurysm
- tumour
-Trauma
-Base of skull fracture
-Arnold-chiari malformation
---cerebellar tonsilar protrusion through teh foramen magnum. May be associated with cerebellar dysfunction.
91
What signs might be found in a patient with an Arnold-Chiari malformation?
CN IX, X, XI, XII dysfunction
Cerebellar ataxia
Upper motor neuron signs in the limbs
92
What causes bilateral 12th nerve palsy?
Motor neuron disease
Arnold-Chiari malformation
GBS
Polio
93
Differential for multiple cranial nerve palsies?
Nasopharyngeal carcinoma
Chronic meningitis - TB, sarcoidosis
GBS - especially the Miller-Fischer variant
Brain stem lesions - e.g. glioma
Arnold-chiari malformation
Trauma
Lesions in the base of the skull - cancer, meningioma, Paget's disease
Mononeuritis multiplex (in the setting of diabetes, or PAN, or ANCA vasculitis)
Myopathies and other neuromuscular diseases
94
What is the classic disease association with bilateral CNVII palsies?
Neurosarcoidosis
95
What are the higher centres features unique to dominant parietal lobe lesions?
Gerstmann Syndrome:
Acalculia
Agraphia
Left-right disorientation
Finger agnosia
96
What is the unique higher centre feature of non-dominant parietal lobe disease?
Dressing apraxia
97
What higher centre features (cortical signs) are seen in non-dominant and dominant parietal lobe disease?
Sensory inattention
Visual inattention
Cortical sensory loss
-loss of graphaesthesia
-two-point discrimination
-joint position sense
-stereognosis
Constructional apraxia (intersecting pentagons)
Parietal lobe defects may also be associated mixed sensory deficits that respect the sensory homunculus of the postcentral gyrus, and visual field defects that correlate with suspected lesions sites (inferior quadrantanopias)
98
What would you look for in a higher centres exam features if you suspect temporal lobe disease?
Memory loss - short term and long term.
The non-cortical signs associated with temporal lobe include visual field defects (superior quandrantanopias).
99
What frontal lobe signs should be looked for in a higher centres exam?
Reflexes - grasp, pout, palmar, mental
Proverb misinterpretation
Smell
Fundi
Gait - unable to lift feet off the ground - a failure to initiate.
100
What is titubation?
A nodding movement of the head or the body. When a person with cerebllar diseases tries to stand still they sway at the waist. This is called titubation. Not to be confused with a positive rhomberg's. There head will also bob up and down.
101
What is Foster Kennedy syndrome?
Visual loss due to compressive optic atrophy in one eye, and papilloedema in the contralateral eye due to raised intracranial pressure. Most commonly caused by frontal lobe meningiomas causing raised ICP. Pseudo FKS can be the result of optic nerve compression from the gyrus rectusm, or diabetic pappilopathy, or unilateral optic nerve hypoplasia.
102
What is a paraphrasia?
Using the incorrect word in a sentence
103
What is a phonemic paraphasia?
Using a word that sounds like the word that was supposed to be used in a sentence (may not actually be a word). E.g. I caught the 'treen' to work today.
104
What is a semantic paraphrasia?
Using a word that is in the same category as the intended word, but is obviously incorrect - "at night, I always make the 'table' before going to sleep"
105
What is a neoligism?
A made up word that is used freely as though it carries some meaning.
106
Where is the arcuate fasciculus?
Temporal lobe
107
What is the name of the structure that is damaged in conductive aphasia?
The arcuate fasciculus
108
In isolated nominal dysphasia, what could the cause be?
Temporal lobe angular gyrus
Also seen in encephalopathies, or the recovery phase from a dysphasia.
109
What sort of speech sounds harsh, strained and hollow?
Pseudobulbar palsy (bilaterlal upper motor neuron lesions impacting speech)
110
What sort of speech sounds nasal, floppy, squashed?
Bulbar palsy - lower moto neuron lesions.
111
When looking for upper limb drift, what does the arms drifting upwards signify?
Cerebeller lesion owing to hypotonia
112
When looking for upper limb drift with eyes closed, what do you expect to see if proprioception is lost?
Drift in any direction, with pseudoathetosis. The effected side(s) just 'search' around.
113
What spinal cord roots are tested with shoulder abduction?
C5 and C6
114
What spinal cord roots are tested with shoulder adduction?
C6, C7, C8
115
What spinal cord roots are tested with elbow flexion?
C5 and C6
116
What spinal cord roots are tested during elbow extension?
C7 and C8
117
What spinal cord roots are tested during wrist flexion?
C6 and C7
118
What spinal cord roots are tested during writst extension?
C6/7/8
119
What spinal cord roots are tested during finger extension?
C7 and C8
120
What spinal cord roots are tested during finger flexion?
C7 and C8
121
What spinal cord roots are tested during finger abduction?
C8 and T1
122
What spinal nerve root is tested when checking biceps refelexes?
C5 and C6
123
What spinal nerve root is tested when checking triceps reflex?
C7 and C8
124
What nerve root is tested when checking brachioradialis reflex?
C5 and C6
125
Hoffman's reflex tests which spinal root?
C8
126
What spinal root dermatome is assessed at the thumb?
C6
127
What spinal root dermatome is assessed when testing the middle finger?
C7
128
What spinal root dermatome is being assessed when testing the 5th finger?
C8
129
Where should you test to look for abnormalities in the T1 dermatome?
The medial arm. Don't go all the way up the underarm, as this is typcally T2.
130
What sesnory spinal level is at the nipples?
T4
131
What sensory spinal level is at the umbilicus?
T10
132
What is fascioscapulohumeral muscular dystrophy and what are it's clinical findings?
Inherited muscular dystrophy. 2 subtypes, though 95% are type 1. Type 1 is a autosominal dominant, tandem repeat disease.
Typical findings are muscle weakness involving the facial muscles (CNVII, CNV), dysphagia, shoulders, upper arms. Scapular winging is typical. Lower body abdominal muscle wasting.
Associated non-muscular findings: retinal vasculopathy. Hearing loss. Cardiac dysfunction. Cognitive impairement. Epilepsy.
133
What spinal nerve root level is tested by having a patient stand on their toes?
S1
134
What spinal nerve root is tested by having a patient stand on their heals?
L4/5
135
What spinal root level allows hip flexion?
L2/L3
136
What spinal root level allows hip extesnion?
L5, S1, S2
137
What spinal root levels allow hip abduction?
L4/L5/S1
138
What spinal root levels allow hip adduction?
L2/L3/L4
139
What spinal root levels allow knee flexion?
L5/S1
140
What spinal root levels allow knee extension?
L3/L4
141
What spinal root level is responsible for ankle plantar flexion?
S1
142
What spinal root level is responsible for ankle dorsiflexion?
L4/L5
143
What spinal rool level is responsible for ankle eversion?
L5/S1
144
What spinal root level is responsible for ankle inversion?
L5
145
What spinal roots are tested with a knee jerk reflex?
L3/L4
146
What spinal roots are tested with an ankle jerk reflex?
S1/S2
147
What spinal root is tested with a Babinski reflex?
S1
148
What dermatome is tested over the ASIS?
L1
149
What dermatome is tested over anterior, superior part of the knee?
L3
150
What dermatome is tested over the anterior medial lower leg?
L4
151
What dermatome is tested over the lateral lower leg, but also over the middle 3 toes?
L5
152
What dermatome is tested over the 5th toe or the heal?
S1
153
What dermatome is tested over the popliteal fossa?
S2
154
What nerve roots is assessed when testing anal tone?
S2-S4
155
What nerve roots provide sensation to the saddle region?
S3-S5
156
What does a wide set gait suggest?
Cerebellar ataxia
157
What does a high stepping gait suggest?
Sensory ataxia or foot drop. Slapping associated with sensory deficits.
158
What does circumduction during a gait exam suggest?
Spacticity
159
What does a festinating gait suggest?
Extrapyramidal deficits - e.g. Parkinson's disease
160
What does a magnetic (feet appear stuck to the ground) gait suggest?
Frontal lobe disorder
161
What are the four classic findings of lower motor neuron lesions?
Weakness
Wasting
Decreased or absent reflexes
Fasciculations
162
What are the five classic findings of upper motor neuron lesions?
Weakness across all muscle groups, but with extensors and shoulder abduction weaker than flexors in the upper limbs, and with flexors weaker than extensors in the lower limbs.
Spasticity
Clonus
Increased reflexes
Upgoing plantars
163
What is Charcot-Marie-Tooth disease? What are it's key clinical features?
Spectum of inherited peripheral neuropathies affecting either myelin (CMT1/CMT3), gap junctions (CMT2), or axons (CMT2) within peripheral nerves.
There are X-linked, dominant, and recessive versions.
Pes cavus - short high arched feet with hammer toes
Distal muscle atrophy due to peripheral nerve degeneration - not usually extending above the elbows or the middle thid of the thighs
Absent reflexes
Slight to no senory loss in the limbs
Thickened nerves
Optic atrophy
Rarely, argyll robertson pupils
164
What is the differential for predominatnly motor peripheral neuropathy?
GBS
Charcot Marie Tooth
Acute intermittent porphyria
Diabetes mellitus
Lead poisoning
Multifocal motor neuropathy
Always consider if a neuromuscular junction disorder or myopathy might be the cause.
165
What is the differntial list for predominantly sensory peripheral neuropathy?
Diabetes mellitus
Carcinoma (paraneoplastic)
Paraproteinaemia
Vitamin B6 inteoxication
Sjogren's syndrome
Syphilis
Vitamin B12 deficiency
Idiopathic
166
Causes of painful peripheral neuropathy?
Diabetes mellitus
Alcohol
Vitamin B12 or B1 (thiamine) deficiency
Carcinoma (paraneoplastic)
Porphyria
Arsenic or thallium poisoning
Hereditry (most are not painful)
167
What are the nerve conduction findings for demyelinating peripheral neuropathies?
Reduced velocity <75% the expected speed
Increased distal latency > 130%
Normal amplitude
168
What are the nerve conduction findings for axonal peripheral neuropathies?
Amplitude <50%
Velocity >70%
169
What is the definition of mononeuritis multiplex?
Peripheral neuropathy involving 2 or more distant named nerves.
170
What is the differential for acute mononeuritis multiplex?
Diabetes
PAN
EGPA
SLE
RA
171
What is the differential for chronic mononeuritis multiplex?
Multiple compressive neuropathies in e.g. hypothyroisdism or deforming arthritis.
Sarcoidosis
Acromegaly
Leprosy
Carcinoma
Idiopathic
172
What is found on examation of a complete brachial plexus lesion?
Lower motor signs effecting the whole arm
Sensory loss of the whole arm
Horner's syndrome
173
What is found on examination of an upper trunk (C5,C6) brachial plexus lesion? (aka Erb-Duchene palsy)
Loss of shoulder movement and elbow flexion
Arm held in the 'waiter's tip position'
Sensory loss is present over the lateral aspect of the arm and forearm and over the thumb
174
What is found on examination of a lower trunk (aka Klumke palsy, C8, T1) brachial plexus lesion?
Claw hand with paralysis of all intrinsic muscles
Sensory loss along the ulnar side of the hand and forearm
Horner's syndrome
175
What is cervical rib syndrome?
It's where a supernumary rib grows from the cervical spine above the clavicle and causes a thoracic outlet obstruction. It can compress the trunks of the brachial plexus and the vascular supply to the arm.
176
What is the differentials for fasciculation?
Benign idiopathic fasciculations
Motor neurone disease
Motor root compression
Spinal muscular atrophy (anterior horn cell degeneration)
Spinobulbar degeneration
177
What are the clinical findings of a radial nerve palsy?
Wrist and finger drop (normal wrist flexion)
Elbow extension weakness if lesion is above the spiral grove
Sensory loss over the anatomical snuffbox
Finger abduction appears weak due to inability to straighten them and separate them
178
What are the clinical findings of a median nerve lesion?
Loss of abductor pollicic brevis strength
-abduct the thumb against resistance to test
Loss of flexor digitorum sublimis with a lesion in or above the cuital fossa
- Ochsner's clasping test - clasp hands firmly, index finger does not flex
Sensory loss over the palmer aspect of the thumb/index/middle fingers and the lateral half of the ring finer.
Innervation of the median nerve
All the muscles in the anterior forearm except for the flexor carpi ulnaris and half of the flexor digitorum profundus. As well as the LOAF muscles in the hand
LOAF
- lateral two lumbricals
- Opponens pollicis brevis
- Abductor pollicies brevis
- Flexor pollicis brevis (although this sometimes has ulnar innervation)
179
What is the differntial aetiology of a median nerve palsy?
Idiopathic
Arthropathy (e.g. RA)
Endocrinopathy (hypothyroidism or acromegaly)
Pregnancy
Trauma or overuse
180
What are the clincal features of an ulnar nerve palsy?
-Wasting of the instrinsic muscles of the hand (excepct for the LOAF muscles - lateral lumbricals, opponens pollicis brevis, abductor pollicis brevis, flexor pollicis brevis)
-Weak finger abduction
-Ulnar claw-like hand (flexed 4th-5th digits when attempting to extend all the finger). The lesion appears less severe when the lesion is further up the arm, as the flexor digitorum provundus becomes involved and the flexion of the 4-5th digits becomes weaker.
- Froment's sign positive: unable to pinch paper with a flat thumb. Also will be weak.
-Sensory loss over the medial half of the ring finger and the entire litte finger (dorsal and palmar aspects)
181
Differential for symmetrical small muscle of the hand wasting?
Anterior horn cell disease
-MND
-Polio
-Spinal muscular atrophies
Myopathy
- myotonic dystrophy
- distal myopathy
Spinal cord lesions
-syringomyelia
-cervical spondylosis with compression of the C8 segment
Trophic disorders
-ischaemia
-arthropathies
-complex regional pain syndrome
182
How do you delineate a C8 root lesion, from a lower trunk brachial plexus lesion and an ulner nerve lesion?
C8 sensation change will extend proximal to the wrist, ulnar lesion will not.
Lower trunk lesions will often have a Horner's (if an axillary mass is responsible)
183
What are the clinical features of a femoral nerve lesion?
Weakness of knee extension (quadraceps paralysis)
Slight hip flexion weakness
Preserved adductor strength
Loss of knee jerk reflexes
Sensory loss involving the inner aspect of the thigh and leg
184
What are the clinical features of a sciatic nerve lesion?
Weakness of knee flexion (hamstrings involved)
Loss of power of all muscles below the knee causing FOOT DROP.
Knee jerk in tact
Loss of ankle jerk and plantar response
Sensory loss along the posterior thigh and total loss below the knee.
185
What are the clinical features of a common peroneal nerve lesion?
FOOT DROP
Loss of foot eversion - BUT PRESERVATION OF INVERSION
Sensory loss over the dorsum of the foot
Importantly, also, ankle jerk reflexes are preserved as the reflex doesn't involve the muslces of the anterior compartment of the lower leg.
186
How do you tell the difference between an L5 radiculopathy and a common peroneal nerve lesion?
Foot drop and loss of ankle eversion is present in both pathologies.
However, INVERSION power is preserved in a common peroneal lesion, and lost in an L5 lesion. Note that foot drop can also be a sciatic nerve pathology, but all ankle movement power will be lost.
187
What is the differential for a foot drop?
Common peroneal nerve palsy
Sciatic nerve palsy
Lumbosacral plexus lesion
L4/L5 root lesion
Peripheral motor neuropathy
Distal myopathy
Motor neurone disease
Precentral gyrus lesion
188
Differential for the paraplegic patient with a sensory level?
Cord compression
- loss of all modalities bilaterally below the level involved
- extrinsic compression spares the perineum, intrinsic lesions will not.
- radicular pain and lower motor neurone weakness are present AT the level of compression.
Transverse myelitis
Anterior spinal artery occlusion
- dorsal column is spared
Multiple sclerosis
189
Causes for the paraplegic patient with arm abnormalities as well?
Cervical spondylosis
Syringomyelia
MND
MS
190
Causes for the paraplegic patient with CN, arm and leg invovlement?
MND
MS
191
Peripheral neuropathy and paraplegia causes?
Subacute combined degeneration of the cord
Freidrich's ataxia
Carcinoma
Hereditary spastic paraplegia
Syphilis
192
What is hereditary spastic paraplegia?
Group of familial diseases with progressive degeneration for corticospinal tracts.
Present with (simple)
- lower limb spasticity, upper motor neurone signs and weakness.
- bladder dysfuntcion
Present with (complex)
- the above, and
- peripheral neuropathies
- cognitive impairment, distal muscle atrophy
- visual loss
- epilepsy
193
What are the clinical features of cervical cord compression above C5?
Uppor motor neuron signs in the upper and lower limbs
Paralysis of the diagphragm occurs if the lesion is above C4
194
What are the motor and reflex clinical features of a C5 myelopathy?
Lower motor neurone weakness and wasting of the rhomboids deltoids, biceps and brchioradialis
Upper motor neurone signs affecting the rest of the upper and lower limbs
Bieps jerks is lost
Supinator jerk is inverted
195
What are the motor and reflex clinical features of a C8 lesion?
Lower motor neurone weakness and wasting in the intrinsic muscles of the hand.
Upper motor neurone signs in the lower limbs.
196
What are the clinical features of thoracic cord lesions above T10?
Intercostal paralysis
Loss of upper abdominal reflexes at T7 and T8
Upper motor neurone signs in the lower limbs
Sesnory level on the trunk
197
What are the clinical motor and reflex features of T10-11 lesions?
Loss of the lower abdominal reflexes and upward displacement of the umbilicus on contraction (Beevor's sign)
Upper motor neurone signs in the lower limbs
198
What are the motor and reflex clinical features of an L1 lesion?
Loss of the cremasteric reflexes (stroking or pinching medial thigh and testes raise 0.5cm or more when normal)
Upper motor neurone signs in the lower limbs
199
What are the motor and reflex clinical features lost with an L4 lesion?
Lower motor neurone weakness and wasting of the quadriceps
Loss of knee jerk
200
What are the motor and reflex clinical features of an L5 or S1 lesion?
Lower motor neurone weakness of knee flexion and hip extension (S1) and hip abduction (L5), and calf and foot muscles.
Knee jerk present
No ankle jerk or plantar response
Anal reflex present
201
What are the motor, sensory and relfex clinical features of an S3-S4 lesion?
No anal reflex
Saddle sensory loss
Normal lower limbs
202
What are the clinical features of combined acute degeneration of the cord?
Symmetrical posterior column loss - ataxic gait
Symmetrical upper motor neurone signs in the lower limbs, but absent ankle reflexes. Knee reflexes are usually exaggerated, but may be absent.
Peripheral sensory neuropathy
Optic atrophy
Dementia
203
What can cause an upgoing planter with loss of reflexes in the lower limbs?
Subacute combined degeneration of the cord
Conus medullaris lesions
Combination of UMN lesions AND cauda equina compression or peripheral neuropathy
Syphilis
Friedreich's ataxia
Diabetes mellitus
Adrenoleukodystropy or metachromatic leukodystrophy
204
What is Brown-Sequard syndrome?
Hemisection of the spinal cord.
205
Where does the spinothalamic tract decussate?
At the level of the spinal cord that it enters
206
Where does the dorsal collumn decussate?
At the medullar.
207
What sensory/motor deficits are seen in Brown-Sequard syndrome?
Spinothalamic loss below the lesion on the contralateral side of the lesion.
Dorsal column loss on the ipsilateral side of the lesion.
Weakness on the ipsilateral side of the lesion.
208
What are the possible causes of Brown-Sequard syndrome?
Multiple sclerosis
Angioma
Glioma
Trauma
Myelitis
Postradiation myelopathy
Note that cord stroke is not on here because its not the way the vascular supply of the cord works.
209
What are the causes of only spinothalamic loss?
Syringomyelia (cape distribution)
Brown-Sequard syndrome (contralateral side)
Anterior spinal artery thrombosis
Lateral medullary syndrome (contralateral to other signs)
Peripheral neuropathy (diabetes mellitus, amyloid, Fabry disease)
210
What is Fabry disease?
Lysosomal storage disease
X linked
Neuropathic limb pain (acroparesthesias), worsened by temp extremes or exertion, onset around 10
211
What causes isolate dorsal column loss?
Subacute combined degeneration of the cord
Brown-Sequard syndreom in the ipsilateral leg
Spinocerebellar degeneration (e.g. Friedreich's ataxia)
Multiple scleroris
Tabes dorsalis (syphilis)
Sensory neuropathy or ganlionopathy
Peripheral neuropathy from diabetes mellitus or hypothyroidism
212
What is the clinical triad of syringomyelia?
Disease o fthe central cavity in the spinal cord
- Loss of pain and temperature over the neck, shoulders and arms (cape distribution)
- amyotrophy (weakness, atrophy and areflexia) of the arms
- Upper motor neurone signs in the lower limbs
213
Differential for proximal muscle weakness?
Myopathic
Neuromuscular junction (e.g. myasthenia gravis)
Neurogenic - motor neurone disease, polyradiculopathy
214
Differentials for myopathy?
Hereditary muscular dystrophy
Congeital myopathies
Acquired myopathies
215
What are the acquired myopathies?
PACE PODS
Polymyositis and dermatomyositis
Alcohol
Carcinoma
Endocrine
-(hyopthyroisim, hyperthyroidism, Cushing's syndrome, acromegaly, hypopituitarism)
Periodic paralysis
Osteomalacia
Drugs
Sarcoidosis
216
What are the causes of combined proximal myoapthies and peripheral neuropathies?
Paraneoplastic syndromes
Alcohol
Connective tissue diseases
217
What are the clinical features of Duchenne's muscular dystrophy?
Strictly X-linked, so only effects Males, or females with Turner's syndrome
Calves and deltoids are hypertrophies early and weak later
Early proximal muscle wakness
Tendon reflexes are preserved in proportion to muscle strength
Severe progressive kyphoscoliosis
Heart disease (dilated cardiomyopathy)
Creatine kinase level markedly elevated
Patients die in the second decade from heart disease typically.
218
What are the clinical features of Becker's muscular dystrophy?
Same as Duchenne's, but onset is later in life and it is less rapdily progressive.
219
What are the features of limb girdle muscular dystrophy?
Shoulder and pelvic muscle weakness
Face and heart muscles usually spared
220
What tests should be done if suspecting myopathy?
Creatine kinase
EMG
ECG
Muscle biopsy
Echochardiogram
221
What are the clinical features of myotonic dystrophy?
Myotonic dystrophic facies
- frontal balding
- dull triangular facial features (hatchet face)
- atrophic temporalis, masseter and SCM
- bilateral partial ptosis
- cataracts
Weak neck flexion
Percussion myotonia - tapping over the thenar eminence
Distal muscle wasting - especially forearm muscles
Mild sensory changes
Gynaecomastia
Testicular atrophy
Diabetes mellitus
Cardiomyopathy
Mental status
222
If myotonia is found, what are the differential diagnoses?
Dystrophia myotonica (typical myotonic dystrophy)
Mytotonia congenita (just the tongue and thenar eminence)
Paramyotonia congenita (episodic myotonia after cold exposure)
223
What are the classic EMG findings of myotonic dystrophy?
Diver bomber effect with needle movemen in the muscle at rest.
224
What ist he order fo the gait exam?
Inspect
Walk normally and turn around quickly
Walk heel to toe (cerebellar disease)
Walk on toes (S1)
Walk on heels (L4/L5)
Squat (proximal myopathy)
Romberg's sign - feet together
--eyes closed (posterior columns), and eyes open (cerebella)
---Proceed to normal lower limb neurology exam
225
What is the differential for unilateral cerebellar lesions?
Space-occupying lesions (tumour, abscess, granuloma)
Ischaemia (vertebrobasilar disease)
Paraneoplastic syndromes
Multiple sclerosis
Trauma
226
What is the diagnosis for bilateral cerebellar lesions?
Drugs (e.g. phenytoin)
Friedreich's ataxia
Hypothyroidism
Paraneoplastic syndrome
Multiple sclerosis
Trauma
Arnold-Chiari malformation
Alcohol
Large space-occupyin lesions
Cerbrovascular disease
Rare metabolic diseases
227
What is the differential for a midline cerebellar lesion?
Paraneoplastic syndromes
Midline tumours
228
What are the most common cancers associated with cerebellar paraneoplastic syndromes?
Small cell lung cancer
Breast Cancer
Lymphoma - particularly Hodgkin's lymphoma
229
Rostal vermis lesions of cerebellum only affect the lower limbs. What's the cause of this typically?
Alcohol
230
What does rebound (rapidly moving the arms up from the side and then stopping when parallel to the ground) test?
Cerebellar function. Overshoot will happen on the affected sides.
231
What cranial nerve dysfunction might also be seen in a patient presenting with cerebellar dysfunction?
If there is a cerebellopontine angle tumour, 5th/7th/8th nerve might be involved. They may also have lateral medullary syndrome.
232
What do midline lesions of the cerebellum cause?
Truncal ataxia - abnormal heel-toe walking
Abnormal speech
233
What are the clinical features of cerebellar ataxia?
Cerebellar signs (bilateral) including nystagmus
Dorsal colum loss in the limbs
Upper motor neuron signs in the limbs, except the ankle reflexes are absent
Peripheral neuropathy
Optic atrophy
Pes cavus
Cardiomyopathy (ECG abnormalities occur in more than 50% of cases)
Diabetes mellitus
234
What are the causes of spastic paraparesis and ataxic paraparesis (upper motor neurone and cerebellar signs combined)?
Spinocerebellar degeneration (e.g. Friedreich's ataxia)
Spinocerebellar ataxia
Arnold-Chiari malformation
Multiple sclerosis
Syingomyelia
Infarction of the upper pons or internal capsule
Lesion at the craniospinal junction
235
How should a Parksinon's disease patient be examined? What will you find?
Inspect - mask like face, pill rolling asymmetric tremor, facial tremors, absence of blinking
Gait - festination, difficulty starting, shuffling, freezing. Propulsion and retropulsion.
Finger-nose testing: should see reduction in the tremor
Upper limb tone: rigidity at the wrist
Test for abdnormal rapid alternating movements - look for involuntary movements produced by dopamine traetment
Test for decriminting movements (baby shark)
Glabellar tap (needs to be done with the finger outside the patients field of view)
Briefly test expressive speech (typically monotonous)
Look at eye movements ?PSP
Ask the patient to write ?micrographia
Test frontal lobe reflexes
Test for postural hypotension
236
What part of the brain is typically diseased in conditions that cause chorea?
The corpus striatum. It's part of the basal ganglia.
237
What's the difference between chorea, hemiballismus and athetosis?
Chorea are non-repetitive, abrupt, involuntary, and is more distal. Typically bilateral.
Hemiballismus is more unilateral, involves rotary movements of proximal joints.
Athetosis is slow, distal writhing movements at rest.
238
Where are lesions that cause hemiballismus?
In the subthalamic nucleus of the contralateral basal ganglia.
239
Where are the lesions that cause athetosis?
In the outer segment of the putamen of the basal ganlgia.
240
What should be examined if chorea is suspected?
Shake hand - assess for variable strength
Ask pt to hold arms out in front of them - note movements
Look at the eyes for
- exophthalmos
- Kayser-Fleischer rings
- conjunctival injection (ataxia- telangiectasia)
Ask the patient to stick out tongue
- look for serpentine tongue
- look for SLE signs (ulcers)
Look for butterfly rash (SLE)
Test knee jerks
- pendular in Huntingtons disease
Higher centres
- associated dementing process
Heart ?signs of rheumatic heart disease
241
Differential for Chorea?
Huntington's disease
Syndenham's chorea (rheumatic fever)
Senility
Wilson's disease
Drugs (phenothiazines, the contraceptive pill, pheytoin, L-dopa)
Vasculitis or connective tissue disedase (esp. SLE)
Thyrotoxicosis (very rarely)
Polycythaemia or other causes of hyperviscosity
Viral encephalitis
242
What are the features of multiple system atrophy P?
Autonomic dysfunction - but less prominent than Shy-Drager
P stands for parkinsonism predominant
Progresses more rapidly than Parkinson's disease
243
What are the features of multiple system atrophy C?
Autonomic dysfunction - but less prominent than Shy Drager syndrome
Parksinonism, but much less prominent than in MSA-C
C stands for cerebellar dysfunction
244
What is shy drager syndrome?
Multiple system atrophy (autonomic dysfunction, parkinsonism) but with autonomic dysfunction as the primary feature.
245
What is corticobasal degeneration?
Parkinsons plus
Alien limb
Cortical dysfunction early
Myoclonus
Death within 10 years
246
What are the classes of Parkinson's drugs?
Levodopa
Dopamine receptor agonists (e.g. ritogotine)
MAO-B inhibitors (e.g. rasagiline)
Anticholinergics for tremor (e.g. benzatropine)
COMT inhibitors - reduce L-dopa GI breakdown
Apomorphine
247
What are the subtypes of motor neuron disease and their features?
Amyotrophic lateral sclerosis - UMN and LMN involvement
Progressive muscular atrophy - LMN predominant
Primary lateral sclerosis - UMN predominant
Progressive bulbar palsy - bulbar predominant
248
What are the important MND mimics?
Syringomyelia - LMN at level of syrinx, UMN below
Cervical myelopathy - LMN at level, UMN below
HIV related myelopathy
Spinal cord tumour
Multifocal motor neuropathy (autoimmune demyelinating neuropathy with distal weakness and atrophy)
249
What antibodies are associated with multifocal motor neuropathy?
IgM anti-GM1 ganglioside abs
250
What needs to be managed in motor neurone disease?
Drooling
Dysphagia
Communication difficulties
Emotional lability
Spascticity
Limb weakness
Respiratory symptoms
Depression
Pain
251
How does riluzole work?
Reduces glutamate release from pre-synaptic terminals
252
What FVC is required for MND patients to be eligible for riluzole in Australia?
FVC > 60%
253
What mortality benefit is there for patients taking riluzole with MND vs placebo?
3 months
254
What are the cardiac complications of myotonic dystrophy?
Prolonged PR or QT
ST and T wave changes
QRS widening
Heart blocks (first degree very common)
SVT
VT
AF (very common)
Mitral prolapse
255
What are the GI manifestations of myotonic dystrophy?
Dysphagia
Reflux
Delayed gastric emptying
Hypomotility
Malabsorption
Overgrowth
Megacolon
256
What are the respiratory manifestations of myotonic dystrophy?
Resp muscle weakness
T2RF during anaesthesia
Increased risk pneumonia
257
What CNs are involved in cerebellopontine angle lesions?
V, VI, VII, VIII
Pts also have cerebellar dysfunction
