Common abnormalities

Muscle wasting can have a multiplicity of different causes (see Table 6.20). In order to determine the anatomical cause of atrophy, it is necessary to assess its distribution; whether it is focal or diffuse, primarily proximal or distal or whether or not the atrophy involves a peripheral nerve or a spinal segment. Conversely, muscle hypertrophy may be occupational or a manifestation of certain rare forms of muscular dystrophy (e.g. Duchenne).

Fascieulations appear as subcutaneous twitches overlying muscle bellies when the muscles arc at rest. They result from disease of lower motor neurones that innervate that particular muscle and are caused by brief contraction of single motor units. They may be coarse or fine in amplitude and are most commonly found in wasted muscles. They can occur in normal people after vigorous exercise. A similar usually benign phenomenon, myokymia, involves fasciculations of the orbicularis oculi. This condition is commonly caused by anxiety and tiredness.

Myoclonus is a sudden shock-like muscle contraction which involves one or more muscles of a whple limb. Myoclonic jerks may be focal or diffuse and may occur singly or repetitively. They may occur in normal people, particularly when falling asleep. Some patients with primary generalised epilepsy experience myoclonic jerks, especially after waking. Less common causes of myoclonic jerks arc rare diseases such as Creutzfeld-Jakob disease, subacute sclerosing panencephalitis, familial myoclonic epilepsies, and anoxic cerebral damage.

Choreiform movements are irregular, jerky, semipurpose-ful and ill sustained. They tend to be multifocal and are classically seen in Huntington's chorea.

Tics or habit spasms are much more stereotyped and localised than choreiform movements, and sometimes can be temporarily resisted at will by the patient

Spinal cord

Fibres for head Internal capsule

Mid-brain

Pons

Medulla

Internal Capsule Fibres

Basilar pari of pons

Decussation

Visual fibres

Sensory fibres

Internal capsule posterior limb

Fibres for lower limb

Fibres 1o motor nuclei of other half of mid-brain Crus cerebri

Fibres for head

6th nerve nucleus 7th nerve nucleus

Fibres to motor nuclei of other half of medulla

Lateral (Indirect) corticospinal tract

Corticospinal (pyramidal) tract

To anterior horn

Fibres for lower limb

Anterior (direct) corticospinal tract

Pyramid

Basilar pari of pons

Decussation

Spinal cord

Visual fibres

Fibres for head Internal capsule

Sensory fibres

Internal capsule posterior limb

Fibres for lower limb

Mid-brain

Fibres 1o motor nuclei of other half of mid-brain Crus cerebri

Corticospinal (pyramidal) tract

To anterior horn

Fibres for lower limb

Fibres for head

Pons

6th nerve nucleus 7th nerve nucleus

Fibres to motor nuclei of other half of medulla

Anterior (direct) corticospinal tract

Lateral (Indirect) corticospinal tract

Medulla

Pyramid

Fig. 6.27 The motor pathways.

Tremor is defined as rhythmic movement resulting from alternating contraction and relaxation of groups of muscles (see Table 6.21). Tremors produce oscillations about a joint or group of joints. The pattern of tremor most frequently seen is rapid and fine in amplitude and is an exaggeration of physiological tremor. It is prominent in patients with hyperthyroidism and some patients who indulge excessively in alcohol, coffee or other drugs. A distal upper limb tremor is a cardinal feature of parkinsonism and characteristically involves a beating of the thumb towards the index tinger. In ils fully developed form, it is of 'pill rolling' type with Ihe thumb moving across the tips of all fingers. Parkinsonian tremor is maximal at rest and reduced by voluntary movement. Intention tremor is absent at res!, present on actively maintaining a position and exacerbated by movement. It is due principally to disorders of the cerebellum or its connections. Much coarser and often more violent tremors usually Involving the upper limb are induced by

Anatomical aetiology

Associated features

Common causes

Lower motor neurone Upper motor neurone

Myopathies Psychological

Muscle atrophy Fasciculation

Reflexes absent or diminished Hypotonia

'Patterned' weakness Little or no muscle wasting Hyperreflexla Hypertonia

Hypokinesia of movement

Muscle wasting (usually proximal) Hypotonia

Tenderness (myositis)

Inconsistent weakness Mo associated features

Peripheral neuropathies Radiculopathies

Anterior horn cell damage (e.g. poliomyelitis) Motor neurone disease

Cerebrovascular disease (e.g. hemiplegia) Spinal injury or disease (e.g. paraplegia) Multiple sclerosis

Hereditary conditions (e.g. muscular dystrophy) Alcohol and other toxins

Stress Anxiety

Compensation claims

TABLE 6.21 Types of tremor

■: ' ■ :: .

Name

Frequency (Hz)

Examples

Rest

Posture

Movement

Action (or postural)

10

Hyperthyroidism

_

+

+

^__Anxiety and fatigue

Intention

5

Cerebellar

-

+

++

Resting

5

Parkinsonism

++

±

±

active movements (action or kinetic tremors) and abolished by rest in patients with multiple sclerosis, cerebrovascular disease involving the midbrain red nucleus (and thus termed 'rubral'-type tremor) or subthalamic nucleus. The last classically causes hemiballismus, in which there arc violent throwing movements of the limbs on one side.

Dystoriic movements are slow and writhing and often lead to sustained abnormal contracture and limb posturing. These are often called torsion spasms and are most commonly seen in spasmodic torticollis, following infantile hemiplegia and in dystonia musculorum deformans. Athetosis describes slow writhing movements of distal parts, usually fingers and toes. Dystonia is typically due to extrapyramidal dysfunction, usually involving the basal ganglia. Palpation is of limited value. Abnormalities include:

• tenderness in inflammatory conditions (myositis)

• 'doughy' in Duchenne's dystrophy as a result of fatty infiltration of the pseudohypertrophied muscles

• 'woody" in some forms of acute muscle necrosis (e.g. alcoholic rhabdomyolysis).

Percussion of muscle bellies may enhance the production of fasciculations, or occasionally elicit sustained contraction in myotonic disorders (percussion myotonia).

Tone

There are also considerable individual variations in muscle tone which may be defined as the resistance felt when a joint is moved passively through its range of movement. In normal people who are relaxed the manipulation of a joint evokes slight 'clastic' type of resistance from the adjacent muscles. The normal degree of this tension can be gauged only by repeated examination of healthy people.

Examination sequence

□ Note any involuntary movement or abnormalities of posture or gait.

□ Inspect the muscles for symmetry and for fasciculation, noting the nature and anatomical distribution of any abnormality.

□ Palpate and/or percuss muscle groups to clicit tenderness or other features.

Tone

□ Passively Ilex and extend each joint in turn; do this slowly at first and then more rapidly to get a feel of muscle tension (Fig. 6.28A).

□ In the upper limbs test muscle tone at the shoulder, elbow joint and wrist joint.

Patella Klonus TestResting Leg
knee. HI Rock the relaxed leg to and fro.

□ In the tower limbs test tone by internally and externally rotating the resting leg (Fig. 6.28B) and by briskly raising the patient's knee off the bed and observing whether the ankle is also raised off the bed.

Knee clonus

□ Sharply push the patella towards the foot while the patient lies supine and relaxed with the knee extended.

□ Following the initial jerk, exert sustained pressure with the thumb and index finger in a downwards direction on the patella.

Ankle clonus

□ Support ihe flexed knee with one hand in the popliteal fossa so that the ankle rests gently on the bed.

□ Using the other hand briskly dorsiflex the foot and sustain the pressure (Fig. 6.29),

Abnormal findings

Abnormalities in tone should be interpreted in the light of other clinical findings.

Hypertonia may be manifest as either spasticity or rigidity. Spasticity is characterised by rapid build-up of resistance during the first few degrees of passive movement and then as the movement continues there is sudden

Upper Motor Neuron Clonus Test

lessening of resistance. Hypertonia is a feature of upper motor neurone pathology. It is usually associated with increased deep tendon reflexes, clonus, an extensor plantar reflex and typical patterns of weakness. It is a common finding in cerebrovascular disease, multiple sclerosis, traumatic spinal injury and degenerative spondylotic myelopathy. Spasticity in the upper limb is frequently more obvious in attempted extension, whereas in the lower limb it is more obvious with attempted flexion. Rigidity is a term used to describe sustained resistance to passive movement. Rigidity is most frequently encountered in patients with Parkinson's disease (who will often have the other manifestations of (his disease such as hradykinesia. tremor, gait and postural abnormalities). The rigidity may be sustained throughout the range of movement or may have a phasic component giving it a jerky feel (cogwheel rigidity), as in parkinsonism.

Hypotonia may be very difficult to discern in a relaxed patient, In the upper limb, hypotonia may be evident from the posture of the outstretched hands, which show flexion at the wrist and extension of the fingers (dinner fork deformity). Hypotonia is encountered in lower motor neurone and cerebellar disorders and in chorea. It is often associated with hyporellexia, muscle wasting and paresis. Hypotonia is also seen transiently in the early phase following capsular cerebrovascular accident in which the plegic limb is alonic prior to becoming spastic and hyper-reflexic. Cerebellar hypotonia is subtle and often difficult to detect but may be evident if knee reflexes are pendular (sec below).

Clonus is a term applied to a rhythmic series of involuntary muscle contractions evoked by sudden stretch of the muscles. If knee clonus is present, the patella will jerk up and down following a solitary jerk stimulus. If sustained ankle clonus is present there will be a rhythmical beating (alternating plantar and dorsiflexton) of the foot for as long as the pressure is maintained.

Dystrophia Myotonica
Fig. 6.30 Muscle wasting in patient with dystrophia myotonica.

Although a few heals of clonus are present in some normal people, sustained clonus indicates damage lo the upper motor neurones and is a 'hard' neurological sign.

In dystrophia myotonica. there is muscle wasting (Fig. 6.30) and the delay in muscle relaxation time gives an impression of abnormal tone.

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Responses

  • nadine
    How do you test for clonus?
    3 years ago

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