INVOLUNTARY MOVEMENTS

1) GAIT 2) INVOLUNTARY MOVEMENTS

Abnormal gait


Seeing a patient walk can be very revealing for neurological diagnosis and is an important element of assessing disability. Patterns of weakness, loss of coordination and proprioceptive sensory loss produce a range of abnormal gaits .

Abnormal gait

Neurogenic gait disorders need to be distinguished from those due to skeletal abnormalities, usually characterised by pain producing an antalgic gait, or limp. Gaits that do not fit either pattern may be due to psychiatric disorders and are usually incompatible with any anatomical or physiological deficit .

Pyramidal gait

Upper motor neuron (pyramidal) lesions cause a gait in which the upper limb is held in flexion and the ankle joint in the lower limb kept relatively extended, the leg is swung outwards at the hip (circumduction). In a hemiplegia, the asymmetry between the affected and normal sides is obvious in walking. In a paraparesis, both lower limbs swing slowly from the hips in extension and dragged stiffly over the ground .This can often be heard as well as seen .

Foot drop

In normal walking, toe strike follows heel strike during the gait cycle. If there is a lower motor neuron lesion affecting the lower limb , weakness of ankle dorsiflexion disrupts this pattern. The result is a less controlled descent of the foot making a slapping noise. If the distal weakness is more severe, the foot will have to be lifted higher at the knee to allow room for the inadequately dorsiflexed foot to swing through, producing a high stepping gait .

Myopathic gait

During walking, alternate transfer of the body's weight through each leg requires careful control of hip abduction by the gluteal muscles. In proximal muscle weakness, usually caused by muscle disease, the hips are not properly fixed by these muscles and trunk movements are exaggerated, producing a rolling or waddling gait .

Ataxic gait

An ataxic gait can occur as the result of lesions in the cerebellum , vestibular apparatus or peripheral nerves

Ataxic gait

Patients with lesions of the central parts of the cerebellum (the vermis) walk with a characteristic broad-based gait, 'like a drunken sailor' (cerebellar function is particularly sensitive to alcohol). Patients with acute vestibular disturbances walk in a similar broad-based fashion, though the accompanying vertigo distinguishes them from those with cerebellar lesions. Less severe degrees of cerebellar ataxia can be detected by asking the patient to walk heel to toe; patients with vermis lesions are unable to do this .

Sensory ataxia

Impairment of joint position sense makes walking unreliable, especially in poor light. The feet tend to be placed on the ground with greater emphasis, in an attempt to increase what proprioceptive input is available. This results in a 'stamping' gait which is often combined with foot drop when caused by a peripheral neuropathy, but it can occur in disorders of the dorsal columns in the spinal cord

Apraxic gait

In an apraxic gait, there is normal power in the legs and no abnormal cerebellar signs or proprioception loss, yet the patient cannot formulate the motor act of walking. This is a higher cerebral dysfunction in which the feet appear stuck to the floor and the patient cannot walk, even though movement is normal on the examination couch. Gait apraxia occurs in bilateral hemisphere disease such as normal pressure hydrocephalus and diffuse frontal lobe disease .

Extrapyramidal gait

Patients with Parkinson disease and other extrapyramidal diseases have difficulty initiating walking and difficulty controlling the pace of their gait . Patients may get stuck while trying to start walking or when walking through doorways (freezing ) .Once started they may shuffle and have problems controlling the speed of their walking and sometimes have difficulty stopping . This produces the Festinant gait ; initial stuttering steps that quickly increase in frequency while decreasing in length .

INVOLUNTARY MOVEMENTS

Rest tremor


This is pathognomonic of Parkinson disease . It is characteristically pill rolling and usually presents asymmetrically.

Physiological tremor

This the most common type of action tremor and occurs at a frequency of 8-12 Hz. It is common in normal subjects and exaggeration occurs in anxiety and in other situations .

Alcohol withdrawal

Mercury ,lead , arsenic
Toxins
B-agonists ,theophylline ,caffeine ,lithium , dopamine agonists ,sodium valproate ,tricyclics ,phenothiazines , amphetamines
Drugs
Thyrotoxicosis ,cushing disease , pheochromocytoma , hypoglycemia
Endocrine
Fatigue
Anxiety


CAUSES OF EXAGGERATED PHYSIOLOGICAL TREMOR

Essential tremor

Essential tremor is distinct from a physiological tremor, although resembling it superficially. It is slower and may become quite disabling. The condition is often inherited, and in some families most obvious during certain specific actions such as writing or holding a glass ; here there is an overlap with focal dystonias . Alcohol often suppresses it, sometimes to the extent that the patient becomes dependent. Centrally acting β-adrenoceptor antagonists (β-blockers) such as propranolol are often effective in treatment.

Intention tremor

This is characterised by oscillation at the end of a movement and typically occurs in cerebellar disease. A more dramatic intention tremor occurs with lesions in the superior cerebellar peduncle (the site of the cerebellar outflow to the red nucleus).Known as peduncular rubral or Holmes tremor ; this is a violent large amplitude postural tremor that worsens as a target is approached. It is common in advanced multiple sclerosis and may be a source of considerable severity

Asterixis (flapping tremor)

Asterixis, the 'flapping' tremor seen in metabolic disturbances, is the result of intermittent failure of the parietal mechanisms required to maintain a posture. Thus, when a patient is asked to hold out the arms with the hands extended at the wrists, this posture is periodically dropped, allowing the hands to drop transiently before the posture is taken up again. Occasionally, unilateral asterixis can be seen in an acute parietal lesion, usually vascular.



Causes of asterixis

Renal failure Liver failure Hypercapnia Acute focal parietal or thalamic lesion

Chorea, athetosis, ballism


These are due to disturbance of balance of activity in the basal ganglia . Chorea (the Greek for 'dance') : Jerky, small-amplitude, purposeless involuntary movements . In the limbs they resemble fidgety movements, and in the face, grimaces; they suggest disease in the caudate nucleus (as in Huntington's disease. Hemiballismus: More dramatic ballistic flying violent movements of the limbs usually occur unilaterally in vascular lesions of the subthalamic structures. Athetosis : Slower writhing movements of the limbs . These are often combined with chorea (and have a similar list of causes) and are then termed 'choreo-athetoid' movements.

Lacunar infarction Arteriovenous malformation

Vascular

Infective / inflammatory

Pregnancy , Oral contraceptive , Thyrotoxicosis Hypoparathyroidism Hypoglycaemia
Endocrine
Levodopa Dopamine agonists Phenothiazines Tricyclics Oral contraceptive
Drugs
Cerebral trauma
kernicterus
Cerebral birth injury
Huntington's disease, Wilson's disease , Neuroacanthocytosis, , Porphyria, Paroxysmal choreoathetosis
Hereditary


CAUSES OF CHOREA

Dystonia

This means sustained involuntary contraction that causes abnormal posture or movement. It may be generalised in various diseases of the basal ganglia or may be focal or segmental, as in spasmodic torticollis when the head involuntarily turns to one side. Other segmental dystonias may cause abnormal disabling postures of a limb to be taken up during certain specific actions, such as in writer's cramp or numerous other occupational 'cramps'. These segmental dystonias can be treated by the administration of botulinum toxin to a few of the responsible muscles.

Tics

Tics are repetitive semi-purposeful movements such as blinking or screwing up of the eyes. They are distinguished from other involuntary movements by the ability of the patient to suppress their occurrence, at least for a short time. An isolated tic may be no more than a mild embarrassment, but may become frequent at certain times in childhood and then disappear. The uncommon syndrome of Gilles de la Tourette consists of a tendency to multiple tics and odd vocalisations, with obsessive behavioural abnormalities. The pathogenic basis is not understood, but there may be some response to major tranquillisers.