Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Oxford Handbook of Clinical Examination > Important neurological presentations > Flashcards

Important neurological presentations Flashcards

1
Q

Neck stiffness: overview of causes

A

Caused by a number of conditions provoking painful extensor muscle spasm, including bacterial and viral meningitis, subarachnoid haemorrhage, Parkinsonism, raised intracranial pressure, cervical spondylosis, cervical lymphadenopathy, and pharyngitis.
No examination should be conducted if there is suspicion of cervical injury or instability.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Neck stiffness: examination

A

Lie the patient flat.
Taking their head in your hands, gently rotate it to the sides in a ‘no’ movement, feeling for stiffness.
Lift the head off the bed and watch the hips and knees- the chin should easily touch the chest.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Neck stiffness: Brudinski’s sign

A

When the head is flexed by the examiner, the patient briefly flexes at the hips and knees- a test for meningeal irritation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Neck stiffness: Kernig’s sign

A

A further test of meningeal irritation.
With the patient lying flat, flex their hip and knee, holding the weight of the leg yourself.
With the hip flexed to 90 degrees, extend the knee joint so as to point the leg at the ceiling.
If ‘positive’ there will be resistance to leg straightening (caused by hamstring spasm as a result of inflammation around the lumbar spinal roots) and pain felt at the back of the neck.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Neck stiffness: Lhermitte’s phenomenon

A

A test for an intrinsic lesion in the cervical cord (not meningeal irritation).
When the neck is flexed, the patient feels an electric shock-like sensation down the centre of their back.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Upper motor neuron lesion

A

Defined as damage above the level of the anterior horn cell- anywhere from the spinal cord to the primary motor cortex.
No muscle wasting (although will have disuse atrophy in long-term weakness).
Increased tone: spasticity (clasp-knife) due to stretch reflex hypersensitivity.
Typical pattern of weakness is ‘pyramidal’: upper limbs = weak abductors and extensors; lower limbs = weak adductors and flexors; brisk tendon reflexes and clonus, up-going plantar response.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Lower motor neuron lesion

A

Muscle wasting, fasciculation.
Reduced tone.
Flaccid weakness.
Reduced tendon reflexes, plantar response may be down-going or absent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Hemiplegia: examination, inspection

A

Are there any scars from a brain biopsy or craniotomy?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Hemiplegia: examination, tone

A

Tone increased unilaterally.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hemiplegia: examination, power

A

If examining the upper limbs, ask the patient to hold out their arms with their palms facing the ceiling.
Ask them to close their eyes.
Note any failure to fully raise and supinate the arm and any pronator drift with the eyes closed.
Power is reduced in a pyramidal distribution: flexors stronger than extensors in upper limb; extensors stronger than flexors in lower limb.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Hemiplegia: examination, reflexes

A

Brisk tendon reflexes on the affected side.

Remember to examine for clonus which may be present on the affected side.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Hemiplegia: examination, sensation

A

There may be sensory loss, usually on the side of the weakness.
If crossed and dissociated pin-prick/vibration and joint position sense, this localises the lesion to the brainstem.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hemiplegia: examination, gait

A

If the patient can walk, gait will be spastic on the affected side with a foot drop, difficulty flexing the knee resulting in swinging the leg round.
A pyramidal posture of the upper limb may be exaggerated.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Motor neuron disease: overview

A

MND is a disease of the anterior horn cells of the motor pathway.
It is progressive and eventually leads to respiratory failure and death.
Most MND is sporadic but there are genetic forms of the disease.
The most common is the autosomal dominantly inherited SOD mutation.
MND may present as 4 different phenotypes: amyotrophic lateral sclerosis (ALS, most common type with classical mix of upper and lower motor neuron features), bulbar presentation (bulbar symptoms with preservation of limb function in early stages, poor prognosis due to early respiratory involvement), progressive muscular atrophy (LMN signs), or primary lateral sclerosis (UMN signs).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Motor neuron disease: inspection

A

Look around the patient for communication aids, walking aids, and wheelchairs.
Look carefully at the limbs for muscle wasting and fasciculation.
Is there a gastrostomy tube in situ?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Motor neuron disease: cranial nerves

A

Patient may be dysarthric.
Facial weakness.
Weakness of neck flexion and extension.
The tongue shows fasciculation.
Ask the patient to move the tongue quickly- a spastic tongue will not fasciculate but will be weak and move slowly.
There is lip, tongue, and palatal weakness: ask the patient to say ‘M, M, M’, ‘L, L, L’, and ‘K, K, K’.
Jaw jerk is brisk.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Motor neuron disease: peripheral nerves

A

On examination of peripheral tone, power and tendon reflexes, there is a mixture of upper and lower motor neuron signs.
Commonly muscle wasting and fasciculation with brisk reflexes and possibly extensor (up-going) plantar responses.
Sensory examination is normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Myotonic dystrophy: overview

A

The myotonic dystrophies are multisystem disorders in which myopathy and myotonia are prominent features.
Myotonia is continued involuntary muscle contraction after voluntary effort has ceased.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Myotonic dystrophy: inspection

A 
Bilateral partial ptosis.
Slack, open mouth due to jaw weakness.
Frontal balding.
Expressionless face.
Cataracts (look with ophthalmoscope).
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Myotonic dystrophy: tone

A

Normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Myotonic dystrophy: power

A

Distal muscle weakness (especially hands and foot drop).
Myotonia: ask the patient to squeeze their hand tightly shut and then quickly release it- note the slow relaxation of the muscles.
Percussion myotonia: tap the thenar eminence with a tendon hammer- the abductor pollicis brevis will contract and very slowly relax.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Myotonic dystrophy: reflexes

A

Reduced or absent.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Myotonic dystrophy: sensation

A

Normal.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Myotonic dystrophy: associated features

A

Cardiac conduction abnormalities and cardiomyopathy.
Testicular atrophy.
Endocrine disturbance (T2DM).
Cognitive difficulties: intellectual and personality deterioration.
Hypersomnolence.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Myotonic dystrophy: type 1

A

Autosomal dominant inheritance with genetic ‘anticipation’ (subsequent generations develop more severe symptoms earlier in life).
It is an unstable trinucleotide CGT repeat on chromosome 19 in the myotonin protein kinase gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Myotonic dystrophy: type 2

A

Autosomal dominant inherited condition with a slightly different presentation to classic MD.
Patients do not have facial weakness.
Limb weakness is proximal rather than distal.
Clinically milder than type 1, although patients also have cataracts and may have cardiac conduction abnormalities.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Parkinson’s disease: overview

A

Parkinsonism is a pattern of symptoms comprising an akinetic-rigid syndrome.
Parkinsonism has a number of causes including drug-induced and other intracranial pathologies.
Parkinson’s disease is a neurodegenerative disease with loss of dopaminergic cells in the substantia nigra with Lewy body formation.
It is currently a clinical diagnosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Parkinson’s disease: inspection

A

Mask-like facies with little or no expression- hypomimic.
Reduced blink rate.
Is there a head tremor?- yes yes or no no, associated with essential/dystonic tremor not Parkinson’s disease.
Speech is low-volume and monotonous.
Examine for tremor with arms at rest and in posture.
PD tremor is asymmetrical, pill-rolling and worse at rest, but can present with an asymmetrical postural tremor.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Parkinson’s disease: tone

A

Examine tone feeling for asymmetrical cogwheel rigidity.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Parkinson’s disease: power/function

A 
Examine repetitive hand movements such as walking the thumb along the fingers.
Encourage the patient to make big, quick movements to be sure of eliciting bradykinesia if present.
Use synkinesis (active movement of opposite limb) to exaggerate tremor, cog wheeling or bradykinesia.
31
Q

Parkinson’s disease: gait

A 
Difficulty initiating gait.
Loss of arm swing on one side.
Shuffling gait.
Difficulty turning.
Unsteadiness/loss of postural reflexes.
32
Q

Abnormal movements: akathisia

A

Motor restlessness with a feeling of muscle quivering and an inability to remain in a sitting position.

33
Q

Abnormal movements: athetosis

A

Slow, writhing, involuntary movements often with flexion, extension, pronation, and supination of the fingers and wrists.

34
Q

Abnormal movements: blepharospasm

A

Intermittent spasm of muscles around the eyes.

35
Q

Abnormal movements: chorea

A

Non-rhythmical, dance-like, spasmodic movements of the limbs or face.
Appear pseudo-purposeful (the patient often hides the condition by turning a spasm into a voluntary movement, e.g. the arm suddenly lifts up and the patient pretends they were adjusting their hair).

36
Q

Abnormal movements: dyskinesia

A

Repetitive, automatic movements that stop only during sleep.

37
Q

Abnormal movements: tardive dyskinesia

A

Dyskinetic movements often of the face (lip-smacking, twisting of the mouth).
Often a side effect of neuroleptic therapy.

38
Q

Abnormal movements: dystonia

A

Markedly increased tone often with spasms causing uncomfortable-looking postures.

39
Q

Abnormal movements: hemiballismus

A

Violent, involuntary flinging movements of the limbs on one side, rather like severe chorea.

40
Q

Abnormal movements: myoclonus

A

Brief, shock-like movement of a muscle or muscle group.

41
Q

Abnormal movements: pseudoathetosis

A

Writhing limb movements (often finger/arm) much like athetosis but caused by a loss of proprioception.
The arm returns to the normal position when the patient notices it straying.

42
Q

Abnormal movements: myokymia

A

Continuous quivering and rippling movements of muscles at rest like a ‘bag of worms’.
Facial myokymia: especially near the eyes.

43
Q

Abnormal movements: tic

A

Repetitive, active, habitual, purposeful contractions causing stereotyped actions.
Can be suppressed for brief periods with effort.

44
Q

Abnormal movements: titubation

A

Rhythmical contraction of the head.

May be either yes yes or no no movements.

45
Q

Abnormal movements: tremor

A

Repetitive, alternating movements, usually involuntary.

46
Q

Spinal cord lesions: complete section of the cord

A

Loss of all modalities below the level of the lesion.

47
Q

Spinal cord lesions: hemisection of the cord, Brown-Sequard syndrome

A

Motor: below the level of the lesion, UMN pattern of weakness on ipsilateral side with brisk tendon reflexes.
Sensory: below the level of the lesion, contralateral loss of pain and temperature sensation, ipsilateral loss of light touch, vibration sense, and proprioception.

48
Q

Spinal cord lesions: posterior column loss

A

Loss of vibration sense and proprioception on both sides below the level of the lesion.

49
Q

Spinal cord lesions: subacute combined degeneration of the cord

A

Posterolateral column syndrome, often due to vitamin B12 deficiency.
Loss of vibration sense and proprioception on both sides below the level of the lesion.
UMN weakness in lower limbs, absent ankle reflexes.
Also peripheral sensory neuropathy, optic atrophy and dementia.

50
Q

Spinal cord lesions: anterior spinal artery occlusion

A

Loss of pin-prick and temperature sensation below the lesion.
Intact light touch, vibration sense, and proprioception.

51
Q

Spinal cord lesions: syringomyelia

A

Longitudinal cavity (syrinx) in the central part of the spinal cord.
Wasting of the small muscles of the hands, ulnar border of upper limb.
Loss of pain and temperature sensation over the neck, shoulders, and arms in a ‘cape’ distribution (look for scars and cuts).
Intact vibration sense, proprioception, and light touch.
Atrophy and areflexia in the upper limbs.
UMN weakness in the lower limbs.
Look also for scoliosis due to weakness of paravertebral muscles.

52
Q

Cauda equina syndrome: overview

A

The cauda equine is the name given the descending nerve roots which extend from the termination of the spinal cord at the conus (~L1) caudally to the final nerve root exits.
Cauda equina syndrome is characterised by: pain in the lower back; bladder and bowel disturbance, sexual dysfunction; saddle anaesthesia; variable paralysis and sensory disturbance of the lower limbs.
Acute herniation of a lumbar disc compressing the cauda equina and causing sphincter disturbance and paralysis is a surgical emergency and needs to be decompressed immediately to prevent long-term consequences.

53
Q

Cauda equina syndrome: inspection

A

Carefully inspect the lower limbs- with long-standing problems there may be muscle wasting. Upper limbs will be normal.
Note the presence of a catheter suggesting bladder dysfunction.

54
Q

Cauda equina syndrome: tone

A

Normal or reduced.

55
Q

Cauda equina syndrome: power

A

Normal in the upper limbs.
Reduced in the lower limbs.
May be complete paralysis or weakness in a nerve root distribution.
May be unilateral or bilateral.

56
Q

Cauda equina syndrome: reflexes

A

Tendon reflexes may be reduced or absent.

Flexor (down-going) plantar responses.

57
Q

Cauda equina syndrome: sensation

A

Saddle anaesthesia (around the perineum and buttocks).
Compression of the sciatic nerve roots.
May be unilateral or bilateral.

58
Q

Disturbance of higher function: parietal lobe lesion

A

Sensory and visual inattention.
Visual field defects.
Agnosias (lack of sensory perceptual abilities): hemineglect; asomatoagnosia; anosognosia; finger agnosia; astereognosis; agraphaesthesia; prosopagnosia.
Apraxias (inability to perform movements or use objects correctly): ideational; ideomotor; dressing.
Gerstmann’s syndrome: right-left dissociation, finger agnosia, dysgraphia, dyscalculia.

59
Q

Disturbance of higher function: temporal lobe lesion

A

Memory loss- confabulation (invented stories and details).

60
Q

Disturbance of higher function: frontal lobe lesion

A

Primitive reflexes.
Concrete thinking (unable to explain proverbs, e.g. ask to explain what ‘a bird in the hand is worth 2 in the bush’ means).
Loss of smell sensation.
Gait apraxia.

61
Q

Myasthenia gravis: overview

A

MG is an autoimmune disease of the neuromuscular junction.
Antibodies bind to the acetylcholine receptor, blocking acetylcholine.
50-60% of patients present with ocular symptoms, but only 10% of patients have isolated ocular MG.
Disease onset is bimodal: young (15-30) or old (60-75).
90% develop generalised MG which can be fatal if the respiratory muscles are affected.

62
Q

Myasthenia gravis: inspection

A

Look carefully at the eyes- is there unilateral or bilateral ptosis? check the pupils- should be equal and reactive.
Are the eyes conjugate as you inspect?
Is there an eye patch indicating diplopia?
Inspection of the limbs will usually be normal.

63
Q

Myasthenia gravis: cranial nerves

A

Diplopia, worsening at the extremes of gaze- ask the patient if they have double vision and the direction of it, e.g. horizontal, vertical, skewed.
Is there any ophthalmoplegia and in which direction of gaze?
Fatiguable ptosis: hold your finger above the patient’s eye-line and ask them to look up at it for 30 seconds, watch their eyes, if fatiguable ptosis and/or upgaze is present, their eyes will slowly fall back and the eyelids will begin to close.
Facial weakness.
Test by asking the patient to screw their eyes shut, purse their lips and open their jaw, all against resistance.
Neck flexion and extension weakness.
Dysarthria.
Dysphagia- ask the patient about swallowing difficulties.

64
Q

Myasthenia gravis: power

A

Fatiguable weakness of the proximal arm muscles.
Test power in shoulder abduction.
Ask the patient to raise and lower their arms 20 times.
Recheck power (it will have weakened).

65
Q

Myasthenia gravis: differential diagnoses

A

Unilateral ptosis and complex ophthalmoplegia: partial 3rd nerve palsy.
Bilateral ptosis: myotonic dystrophy.
Bilateral facial weakness: Guillain-Barré syndrome, muscular dystrophy.
Proximal muscle weakness: myopathy, muscular dystrophy.
Dysarthria: stroke, motor neuron disease.

66
Q

Multiple sclerosis: overview

A

MS is a cell-mediated autoimmune condition characterised by repeated episodes of inflammation of the nervous tissue in the brain and spinal cord, causing loss of the insulating myelin sheath.
UK prevalence is 100-140 per 100,000 with approximately 2500-3000 new diagnoses per year (50-60 per week).
MS is more common in women with female to male ratio 2-3:1.
MS is usually diagnosed in people aged 15-45, but can occur at any age.
4% of people with a 1st degree relative with MS will also develop it.
20% of MS patients have an affected relative.

67
Q

Multiple sclerosis: examination

A

This presentation is highly variable depending on the site of the inflammation with lower and upper motor neuron signs, sensory system deficits, and cranial nerve palsies.
A full and thorough systems examination is essential.

68
Q

Multiple sclerosis: recognised patterns

A

Relapsing/remitting: symptoms come and go, 80% of patients at onset.
Secondary progressive: gradually more or worsening symptoms with fewer remissions- 50% of those with relapsing/remitting develop secondary progressive during the first 10 years of illness.
Primary progressive: from the beginning the symptoms gradually develop and worsen over time (10-15% of people at onset).

69
Q

Multiple sclerosis: clinical symptoms and signs, motor

A

Weakness of variable severity including mono-, para-, hemi- and quadriparesis.
Spasticity resulting in spastic gait.
Facial myokymia.

70
Q

Multiple sclerosis: clinical symptoms and signs, sensory

A 
Dysaesthesic pain.
Paraesthesia.
Numbness.
Lhermitte's sign.
Severe decrease or loss of vibratory sense and proprioception.
Positive Romberg's test.
71
Q

Multiple sclerosis: clinical symptoms and signs, cranial nerves

A

CNV most frequently involved, followed by VII, III and VIII.
Isolated cranial nerve palsies are not frequent.
Combined cranial nerve palsies are rare in MS.
Symptoms might include trigeminal neuralgia.
Signs such as taste and smell dysfunction frequently found if specifically looked for.

72
Q

Multiple sclerosis: clinical symptoms and signs, cerebellar signs

A

Incoordination including dysdiadochokinesis, failure of heel-shin test, ataxic gait, scanning speech, loss of balance.

73
Q

Multiple sclerosis: clinical symptoms and signs, ocular

A 
Reduced viral acuity.
Colour blindness.
Complete loss of vision (1 in 35 cases).
Retrobulbar pain.
Blurred vision.
Diplopia.
Nystagmus.
Internuclear ophthalmoplegia.
Central scotomata and other visual field defects.
Oscillopsia.
Relative afferent pupillary defect.
Optic disc pallor and atrophy.
Uhthoff's phenomenon (worsening of vision in optic neuritis during fever, in hot weather, or after exercise).
74
Q

Multiple sclerosis: clinical symptoms and signs, other

A 
Neuropathic and musculoskeletal pain.
Bladder, bowel, and sexual dysfunction.
Fatigue.
Cognitive and emotional problems.
Heat sensitivity due to loss of thermoregulation manifesting as excess sweating.
etc.

Oxford Handbook of Clinical Examination (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions