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NEUROLOGY > IMPAIRED BALANCE AND INCOORDINATION > Flashcards

IMPAIRED BALANCE AND INCOORDINATION Flashcards

1
Q

What embryological structure does the cerebellum develop from?

A

The metencephalon (a division of the hindbrain)

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2
Q

How is the cerebellum separated from the occipital and temporal lobes?

A

By the tentorium cerebelli (a tough layer of dura mater)

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3
Q

Anatomical structure of the cerebellum?

A

Consists of 2 hemispheres connected by the vermis
Grey matter is on the surface, and is tightly folded forming the cerebellar cortex
White matter is located underneath the cerebellar cortex

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4
Q

4 cerebellar nuclei?

A

Dentate
Emboliform
Globose
Fastigi

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5
Q

3 functional areas of the cerebellum?

A

Cerebro/pontocerebellum (cerebellar hemispheres)
Spinocerebellum (paravermis)
Vestibulocerebellum (vermis)

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6
Q

Function of the cerebrocerebellum?

A

Planning movements and motor learning; receives inputs from the cerebral cortex and pontine nuclei, and sends outputs to the thalamus and red nucleus
Also regulates coordination of muscle activation and is important in visually guided movements

Mostly: fine coordinatiom

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7
Q

Function of the spinocerebellum?

A

Postural tone
Regulating body movements by allowing for error correction
Receives Proprioceptive information also

Mostly postural tone

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8
Q

Function of the vestibulocerebellum?

A

Controls balance and ocular reflexes, mainly fixation on a target; receives inputs from the vestibular system and sends outputs back to vestibular nuclei

Mostyl equilibrium and balance

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9
Q

Blood supply to the cerebellum?

A

Superior cerebellar artery - branch of basilar artery
Anterior inferior cerebellar artery - branch of basically artery
Posterior inferior cerebellar artery - branch of vertebral artery

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10
Q

Venous drainage of cerebellum?

A

Superior and inferior cerebellar veins - drain into superior petrosal, transverse and straight dural venous sinuses

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11
Q

What is “faintness” and what can cause it?

A

The sensation experienced with decreased cerebral perfusion
E.g. getting out of a very hot bath, heavy bout of coughing, before fainting, meds causing postural hypotension

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12
Q

What influences balance?

A

Vision - provide information about surroundings to help understand body’s position relative to its environment
Motor praxis - planning and execution of coordinated movements
Sensory awareness - vision, proprioception, tactile sensations
Cerebellum
Vestibular apparatus - detects changes in head position and movement

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13
Q

What area of the brain is responsible for motor praxis?

A

Frontal lobe

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14
Q

What is motor apraxia?

A

The inability to perform complex motor tasks despite normal power, coordination, sensation and comprehension
Motor disorder caused by damage to the brain - specifically frontal and parietal lobes

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15
Q

Presentations of motor apraxia

A

Magnetic gait - feel as if feet are pulled down to ground by magnet
Unable to make voluntary movements even though you have the physical ability and understanding to do so
Difficulty copying hand gestures
Difficulty miming tasks e.g. mimicking using scissors

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16
Q

Criteria for idiopathic normal pressure hydrocephalus diagnosis?

A

Progressive gait apraxia and balance disturbance
Variable and mild cognitive impairment - dementia and bradyphrenia
Bladder dysfunction / urinary incontinence

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17
Q

Brain scans of idiopathic normal pressure hydrocephalus?

A

Ventriculomegaly - with no sulcal enlargement (not atrophy but sulci are pushed together due to increased pressure)

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18
Q

What causes normal pressure hydrocephalus?

A

Reduced CSF absorption at the arachnoid villi
May be secondary to head injury, subarachnoid haemorrhage or meningitis

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19
Q

Why can peripheral neuropathy cause diffiuclty with balance and gait?

A

Damage to large sensory fibres harms the ability to feel vibration and touch and damage to small sensory fibres harms the ability to feel pain or changes in temperature
All of these factors contribute to balance

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20
Q

Most obvious symptom when there is a lesion in the vermis/flocculonodular lobe of the cerebellum (vestibulocerebellum)?

A

Gaze instability and nystagmus

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21
Q

Most obvious symptom when there is a lesion in the posterior lobe of the cerebellum (cerebrocerbellum)?

A

Dysmetria

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22
Q

Most obvious symptom when there is a lesion in the anterior lobe of the cerebellum (spinocerbellum)?

A

Gait and truncal ataxia

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23
Q

Features of cerebellar dysfunction?

A

Vanish’d

Vertigo
Ataxia
Nystagmus
Intention tremor
Slurred, staccato or scanning speech
Hypotonia
Dysmetria, dysdiadochokinesia

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24
Q

Cerebellar lesions ipsilateral or contralateral?

A

Ipsilateral

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25
Q

What is vertigo?

A

The false sensation that the body or environment is moving
E.g. might feel as if drifting to one side when walking, feeling as if fall is swaying after getting off a boat

26
Q

Pathophysiology of vertigo?

A

Within the inner ear is the vestibular apparatus. It consists of 3 semicircular canals filled with endolumena and these are all orientated in different directions to detect various movements of the head
As the head turns, the fluid shifts inside the canals and this shift is detected by stereocilia in the ampulla. The sensory input of shifting fluid is transmitted to the brain by the vestibular nerve and lets the brainstem and cerebellum know that the head is moving in a particular direction. The vestibular nucleus then sends signals to the oculomotor, trochlear, abudecens nuclei, thalamus, spinal cord and cerebellum
The cerebellum is then responsible for coordinating movement through the body and the vestibular signals also help the CNS coordinate eye movement

Vertigo can be caused by damage to the vestibular system, brainstem or cerebellum which interfere with the physiology above

27
Q

Central and peripheral causes of vertigo?

A

Central:
Posterior circulation stroke
Vertebrobasilar ischaemia
Brainstem - MS, mass, stroke (e.g. Wallenberg syndrome)
Cerebellopontine angle - acoustic neuroma
Cerebellum - stroke or mass
Low CSF

Peripheral:
Viral labrynthitis
Benign paroxysmal positional vertigo
Menierres disease
Vestibular neuronitis
Ototoxicity

28
Q

What is benign paroxysmal positional vertigo?

A

Cystsals of calcium carbonate (otoconia) become displaced into the semicircular canals e.g. my head trauma, age, viral infection, etc
The crystals disrupt the normal flow through the canals = positional vertigo

Acute onset, paroxysmal (<1 min) repeated attacks brought out on by changes in head position e.g. on lying down, turning head
Lasts days-weeks-months
Prone to relapse

Will complain of headaches and stiff neck as they try to stop themselves turning their head

29
Q

What is Ménière’s disease?

A

An excessive buildup of endolumena in the semicircular canals causing higher pressure than normal and disrupting sensory signals
Causes ~hour long attacks of hearing loss, tinnitus, vertigo and sensation of fullness in the ear
Symptoms are not positional
Spontaneous nystagmus during attacks
Overtime hearing gradually deteriorates

30
Q

What is acute vestibular neuronitis?

A

Inflammation of the vestibular nerve
Usually attributed to a viral infection
Acute onset vertigo that improves within a few weeks

31
Q

What is labryinthitis?

A

Inflammation of the labyrinth
Also causes hearing loss (distinguishes it from vestibular neuronitis)
Usually attributed to a viral infection
Acute onset of persistent vertigo that improves within a few weeks - may not be able to get out of bed, associated nausea
No other focal neurological signs

32
Q

Symptoms of central vs peripheral vertigo?

A

Peripheral is sudden onset, lasts seconds-minutes, often hearing loss is present, coordination is intact and severe nausea

Central is gradual onset (other than stroke), is persistent, no hearing loss, impaired coordination and mild nausea

33
Q

What is the HINTS examination?

A

The examination used to distinguish between central and peripheral causes of vertigo

Head Impulse, Nystagmus, Test of Skew

34
Q

What is the head impulse test?

A

patient sitting upright and fixing their gaze on the examiner’s nose. The examiner holds the patient’s head and rapidly jerks it 10-20 degrees in one direction while the patient continues looking at the examiner’s nose. The head is moved slowly back to the centre before repeating in the opposite direction.
A patient with a normally functioning vestibular system will keep their eyes fixed on the examiner’s nose.
In a patient with an abnormally functioning vestibular system, the eyes will saccade (rapidly move back and forth) as they eventually fix back on the examiner.

The head impulse test is positive in peripheral cause of vertigo

35
Q

What is the test of skew?

A

The test of skew (also called the alternate cover test) involves the patient sitting upright and fixing their gaze on the examiner’s nose. The examiner covers one eye at a time, alternating between covering either eye. The eyes should remain fixed on the examiner’s nose with no deviation. If there is a vertical correction when an eye is uncovered (the eye has drifted up or down and needs to move vertically to fix on the nose when uncovered), this indicates a central cause of vertigo.

36
Q

Questions to ask in a vertigo history?

A

Check what they mean by vertigo
Is it rotational or non-rotational?
Are symptoms constant and persistant?
Duration of each attack?
Are attacks brought on by postural change?
Do they veer to one side with walking?
Are symptoms worse with eyes closed or in the dark?
Are attacks periodic with compete resolution in between attacks?
Any associated migraine symptoms, headaches, hearing loss, neurological Sx
Previous history of travel sickness or dislike of rotational fairground rides?

37
Q

What is rombergs test?

A

Standing still with eyes closed
Increased loss of balance is a positive test

The exam is based on the premise that a person requires at least 2 of the following 3 senses to maintain balance whilst standing: proprioception, vestibular function and vision.

38
Q

What is Unterberger’s test?

A

ask the patient to undertake stationary stepping for one minute with their eyes closed. A positive test is indicated by rotational movement of the patient towards the side of the lesion.

Positive in dysfunction of one labrynth e.g. benign paroxysmal positional vertigo
(Imagine there are 2 engines i..e labrynth, if we lose 1 then it will rotate to the side of the dead engine - this is why with eyes closed or pt not concentrating they will veer to 1 side when walking)

39
Q

What is a vestibular migraine?

A

Vertigo can be part of migrainous aura
Can last hours
Is associated with other migrainous features

40
Q

What is an acoustic neuroma?

A

A vestibular schwannoma
A benign brain tumour that grows on the vestibular nerve

41
Q

History for acoustic neuroma?

A

Features can be predicted by the affected cranial nerves:
cranial nerve VIII: vertigo, unilateral sensorineural hearing loss, unilateral tinnitus
cranial nerve V: absent corneal reflex
cranial nerve VII: facial palsy

42
Q

Investigation for acoustic neuroma?

A

MRI of cerebellopontine angle
Audiometry

43
Q

Practical points to advise patients with vertigo?

A

Change positions slowly
Dont walk in darkness
Focus on a point
Have a chair in the shower

44
Q

Management of vertigo?

A

Short courses of vestibular sedatives
Best Tx: Vestibular exercises
Treat associated headaches and neck aches
Practical points e.g. change position slowly, don’t walk in the dark

45
Q

Vestibular exercises?

A

Epley manoeuvre
Brandt Daroff
Semont and Cawthorne Cooksey exercises

46
Q

What is the Epley manoeuvre?

A

A series of head movements to relieve symptms of benign positional vertigo - it dislodges the crusts from the semicircular canals

Sit on bed with head turned 45 degrees to the left, lie down on back at sickly as possible with head hanging over the edge and wait until dizziness resolves. Then turn head 45 degrees to the right wait until dizziness resolves. Turn to lie on your right hand side then turn head slightly to the right so you are facing the floor and wait wait until dizziness resolves. Slowly sit up tilting head down and sit for 15 mins
Repeat

47
Q

What is the Brandt-Daroff exercise?

A

Treatment for benign paroxysmal positional vertigo
Sit up and turn head 45 degrees to the left
Lie down on left side keeping head turned 45 degrees. Stay for 30 seconds
Sit up for 30 seconds
Repeat on right side
Do this a total of 5 times on each side
Sit up and wait till you don’t feel dizzy before standing up

48
Q

What is the Semont exercise?

A

Treatment for benign paroxysmal positional vertigo

art by sitting upright on the edge of a bed. Turn your head 45 degrees to the left (or as
far as is comfortable).
2. Quickly lie down on your right-hand side. Remain in this position for 30 seconds (or until
you no longer feel dizzy).
3. Quickly move to lie down on your left-hand side, keeping your head in the same position
(your head should be facing down on the bed).
4. Return slowly to a sitting position and wait a few minutes.

49
Q

Cerebellar hemisphere lesions cause “insert answer” Ataxia?

A

Peripheral - often described as “finger-nose ataxia”
This is because the lesion affects the cerebrocerebellum which is responsible for cooordinating voluntary movements and motor planning

50
Q

Cerebellar vermis lesions cause “insert answer” Ataxia?

A

Truncal ataxia i.e. Gait

This is because it affects the spinocerebellum which is involves in regulating posture and coordination of body movements associated with proximal limbs

51
Q

Causes of ataxia/cerebella dysfunction?

A

Head injury
Brain infections e.g. encephalitis or meningitis
Strokes, TIA
CP
MS
Chronic Alcohol misuse
Vitamin B12 deficinecy
Brain tumours
Toxic chemicals e.g. mercury
Hypothyroidism
Hereditary causes
Meds e.g. phenytoin
Can be paraneoplastic (anti-Hu antibodies)
Idiopathic late-onset cerebellar ataxia

52
Q

Types of hereditary ataxia?

A

Friedreichs ataxia (most common)- age 5-20
Ataxia-telangiectasia <5 years
Spinocerebellar ataxia
Episodic ataxia

53
Q

Why does an alcoholic cerebellar degeneration cause prominent gait ataxia in the absence of major upper limb, speech or oculomotor problems?

A

As it mainly results in vermian cerebellar degeneration

54
Q

What is ataxia?

A

Clumsy and uncoordinated movements of the limbs, trunk and cranial muscles resulting from pathology in the cerebellum and its connections

55
Q

Cerebellar ataxia symptoms and signs?

A

Unsteady gait with tendency to falls
Impaired hand coordination
Dysarthria or dysphagia
Ocular symptoms e.g. nystagmus, inaccurate saccades, jerkiness on attempted smooth pursuit

56
Q

Investigations for ataxia?

A

Imaging of brain e.,g for stroke
If nothing on imaging… CSF examination e.g. for infections
Genetic testing may be done

57
Q

Typical age for Friedreich’s ataxia?

A

10-15 years old

58
Q

Presentation of Friedreich’s ataxia?

A

Gait ataxia
Kyphoscoliosis
Absent ankle jerks or extensor plantars
Cerebellar ataxia
Optic atrophy
Spinocerebellar tract degeneration
High-arched palate
HOCM
Diabetes mellitus

59
Q

Most common cause of death in pt with Friedreich’s ataxia?

A

HOCM - 90 % of pt have it

60
Q

What is the diagnostic test for benign paroxysmal positional vertigo?

A

A positive Dix-Hallpike manoeuvre - rapidly lower the pt to the supine position with an extended neck
A positive test recreates the symptoms of BPPV and you will see rotatory nystagmus

61
Q

What is Friedreichs ataxia?

A

An autosomal recessive disorder causing loss of function of FXN gene (a mitochondrial gene that normally codes for frataxin)

Causes neurological dysfunction, cardiomyopathy and diabetes mellitus

Many people live until at least 30s and some can live into their 60s or beyond

62
Q

How many clonus beats are normal?

A

<5

NEUROLOGY (16 decks)

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