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Flashcards in Neurological Examinations Deck (28):
1

Stance and Gait Examination

  • Stance – ask the patient to stand with feet together and eyes open (unsteadiness in cerebellar ataxia) and perform Rombergs test (sensory ataxia due to proprioception defect).
  • Gait – ask the patient to walk 10 metres, turn 180° and walk back towards you and then ask the patient to walk heel toes in a straight line (emphasises gait instability). 

2

Describing Gait

  • Stance and Stability - Unsteadiness on standing with the eyes open is common in cerebellar disorders. Instability that occurs or is markedly worse on eye closure is due to proprioceptive sensory loss = sensory ataxia.
  • Posture - of the trunk, upper and lower limbs.
  • Gait - the height the feet are lifted off the floor and the trajectory of the swing phase - is there circumduction - hemi or diplegia.
  • Rate and speed of the gait.
  • Any difficulty initiating or turning.

3

Hemiplegic and Diplegia Gait

  • Hemiplegic gait – caused by a unilateral upper motor neurone lesion – the leg is extended and internally rotated so the foot draws a semicircle on walking – upper limb is adduction of the shoulder, flexion and pronation at the elbow and a fist is made. The other lower and upper limbs are normal.
  • Spastic diplegic – there is flexion at the hips and knees and extension and internal rotation at the ankles due to a bilateral upper motor neurone lesion (so both feet draw circles on the floor).

4

Ataxic Gait

Broad based unsteady gait – tandem walking is impossible due to cerebellar dysfunction.

5

Hypokinetic Gait

Parkinsonian gait – stooped posture, difficulty in initiation, small steps, reduced arm swing, tremor and can develop into a festinant gait (rapid short steps = hurrying gait). The patient may freeze as a doorway or obstacle approaches. Turning involves short steps with a risk of falls.

6

Trendelenburg Gait

Waddling gait - caused by proximal muscle weakness – there are bilateral tredelenburg signs so the contralateral pelvic drops and the patient leans towards the affected side to stabilise. 

7

Disorders of Speech

  • Dysarthria is disturbance of articulation, dysphonia is impairment of voice or sound production from the larynx and dysphasia is a disturbance in understanding or expression words.
  • Dysarthriaextrapyramidal dysarthria causes monotonous speech in Parkinsons while cerebellar dysarthria causes slow or slurred speech (drunk) and myasthenia gravis causes fatiguing speech.
  • Dysphasia expressive or Broca’s dysphasia is characterised in a reduction in the number of words used and non-fluent speech however comprehension is intact. Receptive or Wernicke’s dysphasia is characterised by poor comprehension and although speech is fluent it is usually meaningless.

8

Arms - General Inspection

  • Note posture at rest with arms outstretched - involuntary movements, muscle symmetry or wasting – wasted muscles feel flabby, inflamed muscles may be tender and necrosis produces a woody firm feel.
  • Pronator drift – caused by increased tone in pronator muscles caused by an UMN lesion.

9

Inspection - Muscle Bulk

Lower motor neurone lesions cause muscle wasting and deformity of the limb.

Wasting is not seen in upper motor neurone lesions but atrophy may develop with longstanding lesions.

Muscle disorders usually result in proximal wasting with the exception of dystrophia myotonica (most common muscular dystrophy) in which there is distal wasting.

10

Inspection - Abnormal Movements

  • Fasciculation – irregular ripples or twitches that occurs due to lower motor neurone lesions.
  • Tremor – oscillatory movement resulting from alternating contraction and relaxation of muscles. It can be fast or slow, fine (physiological in anxiety, hyperthyroidism or with excess alcohol or caffeine) or coarse and maximal at rest (Parkinsons), on maintaining posture (benign essential tremor) or on carrying out movement = intention tremor (cerebellar lesion).
  • Dyskinesias – look for evidence of dystonia, chorea, athetosis, hemiballismus or tics.

11

Tone Examination

  • Upper Limb – first shake hands with the patient – flex and extend the wrist, elbow and shoulders.
  • Lower Limb - remind patient to relax, shake knee from side to side and flick knee upwards (without warning) – if the foot leaves the bed then this suggests increased tone. Flex and extend the patients ankle and knee – observe for increased (rigidity) or decreased (flaccidity) tone.

12

Hypotonia

Flaccidity – in lower motor neurone lesions – associated with muscle wasting, weakness and hyporeflexia.

It may also be a feature of early cerebral or spinal shock when paralysed limbs are atonic prior to developing spasticity

13

Hypertonia

In upper motor neurone lesions:

  • Spasticity – velocity dependant resistance to passive movement so detected on quick movements. It is usually accompanied by weakness, hyper-reflexia and is some cases clonus. In a mild form it is detected as a catch at the beginning or end of passive movement.
  • Rigidity – sustained resistance throughout the range of movement and is most easily detected when the limb is moved slowly. In Parkinsons this is known as lead pipe rigidity and in the presence of tremor it may have a jerky feel = cogwheeling.
  • Clonus – a rhythmic series of contractions evoked by sudden stretch of the muscles.

14

Power - Grading

  • Upper motor neurone lesions cause weakness of a relatively large group of muscles such as an entire limb however lower motor neurone lesions can cause paresis of an individual muscle.

Grade power in the following way – using 4+ and 4- is helpful as many patients are in this category:

  • 0 = No muscle contraction visible.
  • 1 = Flicker of contraction but no movement.
  • 2 = Joint movement when effect of gravity eliminated.
  • 3 = Movement against gravity but not against the examiner’s resistance.
  • 4 = Movement against resistance but weaker than normal.
  • 5 = Normal power

15

Power - Upper Limb

  • Shoulder abduction - Deltoid, Axillary, C5.
  • Elbow flexion - Biceps, Musculocutaneous ,C5, C6.
  • Elbow extension - Triceps, Radial, C7.
  • Wrist flexion - Flexor carpi radialis and ulnaris, Median and Ulnar, C8.
  • Wrist extension - Extensor carpi radialis and ulnaris, Radial, C7
  • Finger abduction - Dorsal interossei and ADM, Ulnar, T1
  • Thumb apposition - Abductor pollicis brevis, Median, C8.

16

Power - Lower Limb

  • Hip flexion - Iliopsoas. Femoral, L1 – L2.
  • Hip extension - Gluteus maximus, Inferior gluteal, L5 – S1
  • Knee flexion - Hamstrings, Sciatic, S1.
  • Knee extension - Quadriceps, Femoral, L3 – L4.
  • Ankle dorsiflexion - Tibialis anterior, Deep peroneal, L4.
  • Ankle plantar flexion - Gastrocnemius, Tibial, S1-S2.
  • Extension of great toe - Extensor hallicus longus, Deep peroneal, L5.

17

Reflexes - Grading

Grade each reflex as – absent, + diminished, ++ normal or +++ increased. 

A reflex – an involuntary contraction of a muscle in response to stretch – monosynaptic reflexes.

  • Changes brisk reflexes are a sign of UMN lesion and diminished reflexes are a sign of LMN lesions. Isolated loss of a reflex suggests a mononeuropathy or radiculopathy e.g. in spinal cord disc prolapse.
  • Reflexes can be reinforced by the patient performing isometric contraction of other muscles – Jendrassik’s manoeuvre = hook the fingers and pull apart laterally or by clenching the teeth.

18

Reflexes - Upper Limb

  • Biceps (C5, C6) – patients arm should be partially flexed at the elbow with the palm down. Place you thumb or finger over the biceps tendon and strike your finger with the hammer.
  • Triceps (C6, C7) – support upper arm by holding the wrist and let the patients forearm hang free. Strike the triceps tendon above the elbow with a hammer.
  • Brachioradialis (C5, C6) – have the patient rest the forearm on the abdomen or lap and strike the radius about 1-2 inches above the wrist. Watch for flexion and supination of the forearm.

19

Reflexes - Lower Limb

  • Knee (L2, L3, L4) – have the patient lie down and lift the knee off the bed. Strike the patella tendon just below the patella and note contraction of the quadriceps and extension of the knee.
  • Ankle (L5, S1) – dorsiflex the foot at the ankle and strike the Achilles tendon – watch for plantar flexion.
  • Babinski response (S1, S2) – stroke lateral sole and a positive babinski is extension (abnormal).
  • Knee clonus – with the patient as relaxed quickly push the patella downwards and look for clonus.
  • Ankle clonus – support knee in flexed position and with the patient relaxed quickly dorsiflex the foot.

20

Co-ordination

  • Abnormalities – caused by muscle weakness, proprioceptive loss or extrapyramidal dysfunction.
  • Cerebellar disorders – past pointing (dysmetria) in finger nose test with intention tremor and an abnormal heel shin test in the lower limbs. Dysdiadochokinesis is slowness and disorganisation of rapid alternating movements e.g. hand tapping. There may also be cerebellar ataxia. Differential diagnosis – toxins e.g. phenytoin or alcohol, vascular lesions, trauma and demyelination in MS.

21

Co-ordination - Upper Limb

  • Rebound phenomenon – ask the patient to stretch out their arms in front of them and maintain this position. Push the patient’s wrist quickly downwards and observe the returning movement.
  • Rapid movements – ask the patient to touch the palm of one hand with the dorsum and palm of the other hand and then ask them to touch the end of each finger with their thumb of the same hand.
  • Point to point – ask the patient to touch their nose and then touch your finger which you can move.

22

Co-ordination - Lower Limb

  • Rapid movements – ask the patient to tap you hand with the ball of each foot as quickly as possible.
  • Point to point movements – ask patient to place heel on opposite knee and run down shin to toe.

23

Sensory Tracts

  • Joint position sense (proprioception) and vibration are conveyed in the posterior (dorsal) columns.
  • Pain and temperature sensation are carried by the spinothalamic tract
  • The dorsal column remains ipsilateral up to the medulla whereas spinothalamic fibres cross to the contralateral tract. 

24

Sensory Examination

Demonstrate normal sensation on the sternum before testing light touch with a wisp of cotton wool, superficial pain with a neurotip, temperature with a cold tuning fork and vibration with a 128Hz tuning fork – start at the DIP joint of the 2nd finger or tip of the great toe and proceed proximally.

25

Abnormal Sensation - Periphery

Nerve and dorsal root – peripheral neuropathies tend to affect the lower limbs first often in a glove and stocking distribution. Causes of polyneuropathies:

  • Genetic – Charcot-Marie-Tooth is a hereditary sensory and motor neuropathy.
  • Inflammatory – Guillian-Barre syndrome or connective tissue disorders e.g. RA or SLE.
  • Systemic conditions – diabetes, renal failure, hypothyroidism, acromegaly, sarcoidosis.
  • Drugs and toxins – alcohol, statins, isoniazid, metronidazole, lead, arsenic or mercury.
  • Vitamin deficiencies – vitamins B1, B6 and B12 or vitamin E deficiencies.

26

Abnormal Sensation - Spinal Cord

Traumatic or compressive lesions of the spinal cord cause loss of sensation in a dermatomal distribution below the level of the lesion.

Anterior spinal artery syndrome and syringomyelia affect the spinothalamic tract (pain and temperature) with relative sparing of the dorsal columns.

Brown-Sequard syndrome – half of spinal cord is damaged so patients get ipsilateral motor weakness, loss of vibration and joint position sense (due to dorsal column damage) and contralateral pain and temperature sensation (due to spinothalamic damage).

27

Abnormal Sensation - Intracranial

Cause contralateral sensory impairment due to fibres crossing over.

28

Joint Position

Hold the sides of the thumb or toe, ask patient to close eyes and tell you whether it is up or down.