Single lesions

The Peripheral Neuropathy Solution

The Peripheral Neuropathy Solution

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The extent and nature of the dysfunction will often enable the location of a lesion to be deduced fairly precisely.

Cerebral cortex. Although the cerebral cortex functions in an integrated manner, certain cortical areas are associated with specific functions. The effects of lesions at different sites in the parietal, frontal, occipital and temporal lobes are summarised in Figure 6.51. Impairment of specialised functions results in dementia, dysphasia, apraxia, astereognosis and other forms of agnosia, often associated with lesions in the visual pathway. Conical motor neurones are spread over a wide area and lesions typically affect function in only part of the opposite side of the body. Thus, unless the lesion is very large, paresis confined to one limb (monoplegia) or to one side of" the face is more likely than a hemiplegia.

In contrast, a profound hemiplegia involving face, arm and leg. associated with loss of sensation of all modalities on the paralysed side, suggests a lesion affecting the internal capsule, where the upper motor neurone and sensory pathways are packed closely together.

Brain stem. Lesions arc characterised by ipsilateral impairment of one or more cranial nerves with concurrent contralateral dysfunction in one or more long tracts. The cranial nerve dysfunction will depend on the part of the brain stem affected, A midbrain lesion is suggested by a III nerve palsy; ponline damage by VI and VII nerve signs accompanied by contralateral upper motor neurone signs. Occasionally other tracts such as the spinothalamic or

TABLE 6.26 Signs attributable to lesions in different parts and paths of the nervous system

Upper motor neurone (pyramidal tract) lesions Weakness or paralysis of movement Increase in tone of 'clasp-knife' type Increased amplitude of tendon reflexes An extensor plantar response

Lower motor neurone lesions Weakness or paralysis of muscles Wasting of muscles with fasclculation Reduction In tone

Diminution or loss ol tendon reflexes

Extrapyramidal lesions Resting tremor (especially 'pill-rolling') Rigidity, cogwheel or 'lead pipe' Bradykinesia, expressionless face, festinanl gait

Cerebellar lesions Ataxia of gait Intention tremor of limbs Jerking nystagmus

Dysarthria of staccato or scanning type

Dysmetria and past-pointing

Hypotonia and pendufar tendon reflexes

Smooth movements may be replaced with jerking movements

Generalised neuropathies

Diminution of superficial sensation affecting the distal aspect of limbs with

'stocking' and 'glove' distributions Wasting and weakness of distal limb musculature Early loss of tendon reflexes

Sensory tracts Dorsal columns:

Ataxia of gait and limb movements aggravated by eye closure (positive

Romberg's test) Impaired position sense Diminished appreciation of vibration

Lateral spinothalamic tracts: mpairment of pain and temperature sensation

Muscles

Wasting and weakness, usually proximal Reduction In reflexes when muscle wasting is marked

Cerebral cortex dysfunction Dysphasia and dyscalculla Right and left disorientation Astereognosis, sensory inattention Apraxia

Amnesia and cognitive disorders Visual field homonymous defects Hemiparesis, monoparesis sympathetic pathways are interrupted. Examples of lesions involving the midbrain, pons and medulla are given in Figures 6.52 and 6.53 (see also Fig. 6. IS)).

Stroke disease. Cerebrovascular accidents (strokes), due to either cerebral infarction or haemorrhage comprise the

2 Parietal lobe

Dominant side

FUNCTION Calculation Language Planned movement Appreciation of size, shape, weight and texture

1 Frontal lobe

FUNCTION Personality Emotional response Social behaviour

LESIONS Disinhibition Lack of initiative Antisocial behaviour Impaired memory Incontinence Grasp reflexes Anosmia

4 Temporal lobe Dominant side FUNCTION Auditory perception Speech, language Verbal memory Smell

LESIONS

Dyscalculia

Dysphasia

Dyslexia

Apraxia

Agnosia

Homonymous hemlanopia

Non-dominant side FUNCTION Spatial orientation Constructional skills

LESIONS

Neglect of non-dominant side Spatial disorientation Constructional apraxia Dressing apraxia Homonymous hemianopia

Constructional Apraxia
3 Occipital lobe

LESIONS

Dysphasia Dyslexia Poor memory Complex hallucinations (smell, sound, vision) Homonymous hemianopia

Non-dominant side FUNCTION Auditory perception Music, tone sequences Non-verbal memory (faces, shapes, music) Smell

FUNCTION Analysis of vision

LESIONS

Homonymous hemianopia Hemianopic scotomas Visual agnosia Impaired face recognition (prosopagnosia) Visual hallucinations (lights, lines and zig-zags)

LESIONS

Poor non-verbal memory Loss of musical skills Complex hallucinations Homonymous hemianopia

Fig. 6.51 Features of localised cerebral lesions.

commonest neurological abnormality seen in medical wards. Strokes may affect the cerebral cortex or the brain stem. Table 6.27 shows the clinical features of stroke in different arterial territories subserved by either the internal carotid or vertebral arteries.

Spinal cord. Damage is localised by correlating motor, sensory and reflex changes. Upper motor neurone signs arising from cord lesions are often, but not always, bilateral. Their presence helps to locate the site of lesion very roughly. If they are present in the arms the lesion lies above the fifth cervical segment: if the abdominal reflexes arc pathologically absent, a segment above Ihe eighth thoracic is implicated. Pyramidal tract signs in the legs indicate a lesion above theconus medullaris.

The site of spinal damage is localised more precisely if the lesion also involves the anterior horn cells or motor roots, thereby causing lower motor neurone signs, with weakness and wasting in a segmental distribution. Sensory signs often help to delineate the position of cord lesions. Impairment of sensation over a segmental dermatome will indicate the level of a lesion. Interruption of sensory tracts may give rise to an upper level of sensory loss which roughly corresponds to the site of the spinal lesion hut which is often at a more caudal level. Spinal cord lesions which disrupt reflex arcs with loss of tendon reflexes indicate the segments which have been damaged.

Often the segmental level and the cross-sectional areas of a spinal cord lesion may be gauged (Fig. 6.54). Below a hemisection of the cord on the ipsilatcral side there will be found (1) upper motor neurone signs. (2) impaired joint position and vibration senses and sometimes (3) signs of

Superior colliculus

Aqueduct

Substantia nigra

- - . Corticospinal (pyramidal) tract

Decussation of superior cerebellar peduncles

Red nucleus

111 nerve nucleus

Medial longitudinal fasciculus

Hi nerves

Cerebellar Peduncles

Midbrain

Fig. 6.52 Lesions of midbrain. Lesions at 1. (e.g. pressure from a pineal tumour) cause weakness of upward gaze which may first be manifest as nystagmus in a vertical plane. Lesions at 2. produce bilateral, partial lesions of the III nerve and anterior internudear ophthalmoplegia (p. 202, damage to medial longitudinal fasciculus). Lesions at 3. cause Ipsilateral III nerve palsy and contralateral cerebellar signs (damage to decussating cerebellar peduncles) and/or tremors and athetoid movements (damage to red nucleus). Lesions at 1. cause ipsilateral III nerve signs and contralateral pyramidal Involvement. Lesions at 5. cause bilateral pyramidal signs. Lesions which aflect the midbrain Immediately below this level also implicate the IV nerve.

- - . Corticospinal (pyramidal) tract

Decussation of superior cerebellar peduncles

Red nucleus

111 nerve nucleus

Aqueduct

Medial longitudinal fasciculus

Substantia nigra

Hi nerves

Midbrain

Medulla Olive

Medulla

IV ventricle Spinal tract and v nucleus Inferior cerebellar peduncle X nerve and nuclei Central sympathetic pathway Spinothaiamic tract Olive Corticospinal tract

Medulla

Fig. 6.52 Lesions of midbrain. Lesions at 1. (e.g. pressure from a pineal tumour) cause weakness of upward gaze which may first be manifest as nystagmus in a vertical plane. Lesions at 2. produce bilateral, partial lesions of the III nerve and anterior internudear ophthalmoplegia (p. 202, damage to medial longitudinal fasciculus). Lesions at 3. cause Ipsilateral III nerve palsy and contralateral cerebellar signs (damage to decussating cerebellar peduncles) and/or tremors and athetoid movements (damage to red nucleus). Lesions at 1. cause ipsilateral III nerve signs and contralateral pyramidal Involvement. Lesions at 5. cause bilateral pyramidal signs. Lesions which aflect the midbrain Immediately below this level also implicate the IV nerve.

vasomotor disturbance. On the contralateral side there will be reduced sensation to pain and temperature This composite picture is called the Brown-Siquardsyndrome.

Peripheral nerve. The most common causes of damage to a single peripheral nerve (mononeuropathy) are entrapment especially in fibro-osseous tunnels (e.g. carpal tunnel syndrome), trauma (e.g. radial nerve palsy), diabetes mellitus (e.g. femoral nerve palsy) or in obesity (e.g. meralgia paraesthetica). Symptoms and signs of some

Fig, 6.53 Lesions of the medulla. Lesions affecting the lateral medulla 1. (e.g. thrombosis of the posterior inferior cerebellar artery) cause ataxia and intention tremor on the ipsilateral side; jerking nystagmus on turning the eyes to the side of the lesion (damage to the spinocerebellar tract in the inferior cerebellar peduncle); analgesia on the ipsilateral side of the face and contralateral limbs (affection of spinal tract of V nerve and the lateral spinothalamic tract); Horner's syndrome (involvement of the central sympathetic pathway); dysphonia. dysphagia and weakness ol soft palate and paralysis of the vocal cords on the side of the lesion (damage to the X nerve). Lesions affecting the paramedian area 2. (e.g. infarction) cause a crossed paralysis - wasting and fasciculation of ipsilateral side of tongue (damage to XII nerve) and contralateral pyramidal signs.

common entrapment neuropathies are summarised in Table 6.28.

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Responses

  • birikti
    What type of viruses cause lesion on the lower motor root nerves?
    8 years ago
  • klaudia
    What causes contralateral cerebellar lesions?
    8 years ago

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