Case 7: basics of neurology Flashcards
1
Q
Causes of cerebellar ataxia
A
- Acute: Vascular, alcohol, drugs (e.g. phenytoin), lithium, cerebellitis, cerebellar stroke
- Sub-acute: Toxic/nutritional (medicine/ B12), inflammatory, neoplastic and paraneoplastic (distant cancer)
- Chronic: Degenerative conditions (MSA, Friedrich’s Ataxia, chronic alcohol use, diabetes, B12 deficiency
2
Q
UMN versus LMN weakness: areas affected
A
- UMN: cortical, spinal
- LMN: plexus, nerve, NMJ, muscle
3
Q
Types of weakness
A
- Neuromuscular weakness: Less than expected force generated from a movement. Varies between individuals
- Constitutional weakness: Generalized fatigue and inability to carry out tasks due to systemic illness or frailty
- Paresis vs plegia: Weakness (paresis) as opposed to paralysis (plegia)
4
Q
Distribution of muscle weakness
A
- Hemi: One side- usually CNS (UMN) in origin with rare exceptions i.e. stroke or spinal pathalogy
- Mono (paresis): Weakness of one limb
- Paraparesis: Weakness of both limbs (typically legs): i.e. LMN (GBS) or spinal cord issue
- Tetra/quadriparesis: All four limbs involved
- Also bulbar (speech, swallowing), axial/truncal (respiration and balance)
5
Q
UMN pathology examination: CNS (brain and spinal cord)
A
- Tone: increased- spastic (velcity dependent- cog wheel rigidity) or rigid (same stiffness all the way through movement- seen in extrapyramidal i.e. parkinsons)
- Increased reflexes
- Babinski/Plantar reflex: positive, upgoing
- Pathological reflexes: Hoffman’s sign
- Other: pronator drift (cortical or high spinal problems), clasp knife response (to removal of force)
- Either Cortico-basal or cortico-spinal
6
Q
LMN pathology examination: plexus, nerve, NMJ and muscle
A
- Tone: decreased or flaccid (can say not increased)
- Reflexes: decreased/absent
- Babinski/Plantar reflex: negative/ down going
- Other: muscle wasting and fasciculations possible
- Causes: neuropathy (nerve damage- sensory or motor), neuromuscular junction (cant sustain strong movement (fatiguability)- often vision (ptosis), and speech), plexus, nerve root, muscle (just motor)
7
Q
Pyramidal weakness
A
- Cortico-spinal or cortico-bulbar weakness
- Arm flexors stronger than extensors: arm bent, hand spastic or floppy often of little use
- Leg extensors stronger than flexors: walks on tiptoe or outside of foot on affected side
- Is Hemiplegic in stroke patients
8
Q
Proximal weakness
A
- Lower motor neurone pattern of weakness. See it mostly in muscle disease and some nerve disease
- Weakness of shoulder abduction (more then distal), weakness of hip flexion
- Difficulties climbing stairs, combing hair, standing up from a seat
- Waddling gait (Trendelenberg’s)
- Many causes-tend to affect muscle rather than nerve: Iatrogenic (long term steroid use), Inflammatory (myositis), Inherited myopathy (Duchenne’s), vitamin D and thiamine deficiency
9
Q
Distal weakness
A
- Weakness starting in hands and feet- such as foot drop
- If painless: MS, MND
- If painful: peripheral neuropathy, vasculitis, inflammation of nerve
- Can be caused by knee crossing and trapping the common peroneal nerve
10
Q
Functional weakness
A
- May be fluctuant/not in keeping with disease patterns
- Patient may find it hard to move limb when focussing but can when distracted
- Patients can describe disassociation
- Hoover’s sign
11
Q
MRCP weakness scale
A
- 5 – normal
- 4 – weak, but some ooommphff needed to overcome the patient
- 3 – very weak, you can beat them with little effort: can just raise limb against gravity
- 2 – so weak that the power would only be useful to an astronaut: can move a bit but not completely against gravity
- 1 – a flicker only
- 0 – nil points
12
Q
What’s involved in balance?
A
- Vision: to see wher we are in space
- Vestibular System: semicircular canals to determine which way we are facing
- Proprioception: muscle spindles (measuring degree of muscle length change) to determine where limbs are in space
- Cerebellum integrates all this information and coordinates downward control from the cerebral hemisphere. Helps to facilitate and regulate eye movements, anticipate future limb position and modulating planned or ongoing movement with sensory information.
13
Q
Different ways to describe dizziness
A
- Ataxia: feeling unsteady, not knowing where they are putting their feet. Tending to fall over from starting or on mobilisation. Due to problems in the peripheral sensory system or cerebellum
- Vertigo- feeling of spinning, rotational motion, can cause nausea. Due to problems in the vestibular system, cerebrum or cerebellum
- Pre-syncope- light-headedness, feeling of faintness, the world going grey and distant. Can feel like they are about to go down, can feel unwell. Due to issues in the autonomic system, cardiovascular system or both
14
Q
Nystagmus
A
- Uncontrolled eye movement
- Would be right sided nystagmus if the eye moves to the right fast and slow to the left
- Bengin Proxysmal Positional Vertigo (BPPV) gives a vertical up-down and torsional (rotational) nystagmus on dix-hallpike.
- Vestibular neuronitis gives a left-right nystagmus worse on gazeaway fromthe affected side i.e. a right-sided problem would cause a nystagmus worse on leftward gaze (and leftward would be the fast phase of the nystagmus)
- A central cause of nystagmus can give a gaze-evoked nystagmus with no obvious unilateral component, can also have vertigal nystagmus
15
Q
Nystagmus tests
A
- Dix-hallpike
- Head impulse test: shows corrective saccade (dont do if neck problems). Done in the HINTS test
- Unterberger test: shows vestibular dysfunction
16
Q
Types of ataxia
A
- Sensory Ataxia - Where the unsteadiness comes from proprioceptive defects in the sensory fibres, dorsal root ganglion or dorsal column. A positive Romberg’s indicates sensory ataxia
- Cerebellar Ataxia -Where unsteadiness comes from disease affecting the cerebellum. Causes DANISH
17
Q
Vestibular causes of dizziness
A
- Triggered Episodic Vestibular Syndrome -Discrete episodes of minutes or hours of dizziness, precipitated by a specific trigger e.g. BPPV, Orthostatic Hypotension
- Spontaenous Episodic Vestibular Syndrome -Discrete episodes with no clear trigger e.g. Vestibular migraine, Meniere’s
- Post-Exposure Acute Vestibular Syndrome -Persistent dizziness lasting days to weeks with history of adverse event such as drugs or trauma e.g. aminoglycosides, head injury
- Spontaenous Acute Vestibular Syndrome -Persistent dizziness lasting days to weeks with no clear history of precipitating event e.g. vestibular neuronitis, posterior circulation stroke
18
Q
BPPV
A
- Middle-aged or older patient
- Feeling of ‘spinning’ when turning in bed or when turning suddenly, tend to be short-lived
- ++ Nauseous when this occurs
- Nystagmus (vertical and torsional) noted on Dix-Hallpike
- Treated through Epley manoeuvre
- No further testing required if not suspicious for a different cause
- Patients can have vestibular physiotherapy for symptoms
19
Q
Vestibular neuronitis
A
- Spontaneous, acute, constant vertigo
- Resolves after a week. Can cause intense ongoing nausea and vomiting
- Often preceding infection
- Nystagmus: horizontal and unidirectional. Worse on gaze away from affected side. Positive head impulse test
- Management: Anti-emetic (Prochlorperazine), treat underlying condition
20
Q
Labyrinthitis
A
- Same as vestibular neuronitis but also acts on cochlear- will have hearing loss
- Add corticosteroids for hearing loss (prednisolone for 10-14 days)
