Disorder motor and / or sensory of a member is a frequent reason for consultation. It requires the first to distinguish between the achievement of the ways of the motor and / or sensitivities and non neurological disorder. The topographic diagnosis based on clinical characteristics of the motor disorder and / or sensitive is the second step. Only he will guide further investigations.
Disorder motor and / or sensory of a Member may recognize non neurological causes and evoke:
– A musculoskeletal origin before the painful nature of the mobilization of a member or to dodge a limp;
– Arterial vascular before a painful intermittent claudication in patients with vascular risk factors;
– A psychogenic origin to the ground and a possible trigger emotional, lack of systematic neurological motor deficit and / or sensitive, the dissociation between the target deficit and functional disability, the “consistency” of the motor deficit who yields by at shots and often varies from one examination to another.
PLACE OF TESTING IN THE EXPLORATION OF MOTOR DEFICIT AND / OR SENSE OF MEMBERSHIP:
The additional investigations depend topographical etiological hypotheses and possibly developed from the interrogation and clinical examination.
The magnetic resonance imaging (MRI) is the examination of choice when it is suspected intracranial lesion or intraspinal whether vascular, tumor, inflammatory or infectious.
It also provides a picture of intracranial vessels (arteries and veins) and cervical vessels for intracranial.
The scanner keeps guidance in traumatic pathology and in case of cons-indication to MRI (pacemaker, certain metallic foreign bodies).
Lumbar puncture is indicated in cases of inflammatory disease of the central nervous system, polyneuropathy suspected, of infectious or neoplastic méningoradiculaire reached.
The electromyogram is essential for the study of peripheral neuropathies. In focal neuropathies confirm the exact topography of nerve pain. In polyneuropathies there distinguishes those of axonal mechanism (most toxic metabolic neuropathies or deficiency, neuropathies with vasculitis or infiltration, most paraneoplastic neuropathies and neuropathies associated with systemic diseases, neuropathies amyloid, some neuropahies dysproteinemias certain neuropathies inherited) from those of demyelinating mechanism (the polyradiculoneuritis, polyneuropathy associated with IgM, some inherited neuropahies).
The electromyogram is also necessary in case of myogenic achieving suspicion or to search for neuromuscular blockade.
Muscle biopsy allows histological confirmation of peripheral neurogenic or myogenic process and can make arguments for the etiological diagnosis.
Neuromuscular biopsy is conceivable that if clinical sensory impairment and electromyography because, unlike muscle biopsy, it can be troublesome (hypoesthesia sequelar area on the dorsum of the foot, difficulties healing).
DEFICIT OF CENTRAL ORIGIN:
Motor deficits by achieving the main driving route may be the consequence of a breach of the first neuron that is the motor cortex to the cranial nerve nuclei and the anterior horn of the spinal cord or of the second neuron will of the anterior horn neuromuscular junction.
Reaching the first neuron determines a central pyramid called or motor impairment.
The deficit prevails in the end, to shorteners the lower limb extensor to the upper limb. The deficit is accompanied by a conservation or exaltation of tendon reflexes and the lower limb of a Babinski sign. Initially, or secondarily in case of sudden onset, the pyramidal deficit is accompanied by an increased muscle tone that predominates in the lower limb extensor and flexor pronator and the upper limb. This is characteristic of spasticity pyramidal syndrome: the imposed motions encounter resistance whose intensity increases with the degree of stretch, which gives it a resilient character, the member returning to its initial position as soon as it is abandoned. When the movement against continued resistance, it can suddenly give way to a knife blade. A recent acute injury of the pyramidal tract is initially accompanied by hypotonia and a weakening of the tendon reflexes.
Topography of the lesion:
The breakdown of the deficit and the associated signs suggest the topography of the lesion.
Hemiplegia usually sign a brain impairment. It may sit in the cerebral hemispheres and then often accompanies disorders of the higher functions that are more marked if the infringement is cortex.
Pure motor hemiplegia is usually the result of sub cortical involvement.
When hemiplegia is linked to a brain stem injury can integrate into an alternate syndrome (diagnosed with cranial nerve, contralateral hemiplegia). Below the top of the protuberance hemiplegia has no ipsilateral central facial reached.
Rarely hemiplegia may correspond to the cervical cord injury. In this case there is no facial involvement, the deficit in proprioception is ipsilateral to the lesion and thermoalgique sensory deficit is contralateral to the lesion and therefore the motor deficit (Brown-Sequard syndrome).
Paraplegia or tetraplegia:
Quadriplegia or paraplegia are usually the consequence of a spinal cord lesion.
In this case the pyramid reached joins willingly to a peripheral lesion syndrome, a superficial sensory disorder with a higher level and sphincter disturbances.
Exceptionally paraplegia can be the result of a bilateral lesion of the paracentral lobule.
Monoplegia a member corresponds to a usually cortex contralateral brain injury. Isolated lower limb involvement may also be the consequence of a dorsal spinal cord injury (ipsilateral deep sensory disturbance, sensory disturbance contralateral thermoalgique).
The mechanism of injury is actually approached primarily by questioning which specifies the field and the installation mode.
Sudden onset is suggestive of ischemic or hemorrhagic vascular mechanism in the brain or spinal cord, even more so if there are vascular risk factors.
Acute or subacute facility is more in favor of an infectious origin (fever) or multiple sclerosis (age less than 50 years, multifocal involvement, changes in spurts).
A progressive installation argues for an expansive intracranial process (intracranial hypertension, epilepsy) or spinal cord compression (spinal signs).
Posttraumatic beginning evokes a brain or spinal cord contusion, an epidural hematoma (short free interval), a chronic subdural hematoma (free interval of several weeks).
A slow evolution suggests amyotrophic lateral sclerosis (pure motor semiotics association with peripheral signs, twitching), a familial spastic paraplegia (family background).
Sensitivity impairment associated:
A sensory impairment of central origin often accompanies motor deficit. Some features, topography feature worth considering.
Consecutive sensory disturbances to a parietal lesion often predominate on the discriminative abilities: sense position precise location of a stimulus, spatial discrimination of two stimuli, stereognosis. It may be associated sensory extinction. Attaining elementary sensitivities is usually limited to hypoesthesia.
Consecutive sensory disorders in thalamic lesions are related to the achievement of the posterior ventrolateral nucleus. The anesthesia or hypoesthesia of the contralateral side of the body covers all the same sensory modalities if the discriminative capacity are most affected. A Cheiro-oral topography is possible. Pain may occur secondarily.
They are continuous with paroxysmal reinforcements. They are usually accompanied by a hyperpathia: painful stimuli normally not felt algic.
Consecutive sensory disorders with damage to the brain stem are often separated. The lateralized lesions of the bulbar or pontine region result in a sensory syndrome alternates: thermal and painful hemianaesthesia of hémicorps opposite the lesion reached the spinothalamic tract, thermoalgique anesthesia ipsilateral hemifacial reached by the descending root neuralgia (Wallenberg syndrome). The above lesions located in the brainstem are responsible for non-differentiated sensory disorders because both sensory pathways converge on the posterior ventrolateral nucleus of the thalamus.
The disorders resulting from spinal cord injury depend on the topography of the lesion.
A lateral lesion of the spinal cord determines a Brown-Sequard syndrome (see above). Intramedullary lesion determines a syringomyelic syndrome dissociated anesthesia thermoalgique suspended as a result of the interruption of sensory fibers that cross the dorsal horn to the contralateral spinothalamic tract, which can associate an abolition of tendon reflexes and segmental deficit with muscular atrophy when the lesion extends to the anterior horns.
The most common cause is the malformation syringomélie. Other causes, vascular, trauma, tumor, are rarer.
The predominant involvement of the posterior columns (posterior cord syndrome) is characterized by a rich paresthésiante semiotics (tingling, skin cardboard sensation, vise, like walking on cotton), proprioceptive ataxia and reviewing disorders discriminative sensibility and sense of joint position while the thermal and pain sensitivity is preserved. The causes are many: inflammatory (MS), compressive, more rarely vascular.
The association with a pyramidal syndrome reached by the lateral columns performs a combined degeneration of the cord (B12 deficiency, vacuolar myelopathy of AIDS). Concomitant reached the posterior columns and posterior root realizes the post-radiculo cordonal syndrome that combines the posterior cord syndrome a aréfl Exie osteo-tendon, shooting pain and trophic disorders. The classic etiology but is now rare in tabes. It is also found
in paraneoplastic damage and some spinocerebellar degeneration (Friedreich’s disease).
DEFICIT ORIGINAL DEVICE:
Reaching the second neuron of the main driving route determines a so-called peripheral motor deficit. The peripheral paralysis is characterized by the association of the deficit areflexia in the territory concerned, hypotonia, secondary atrophy and if some twitching. The peripheral nervous system is rarely purely motor, it is most often associated with a subjective sensory impairment and / or objective that can exist alone and is usually not separated. Again semiotics is essentially dependent on the topography of lesions.
Reaching the motor neuron in the anterior horn:
Reaching the anterior horn motor neuron performs a pure motor impairment. In ALS, the disease is often diffuse and partners with a pyramidal syndrome that accounts for the preservation or even the exaltation of tendon reflexes in amyotrophies territories.
Reaching the sensory ganglion (ganglionopathie):
Reaching the sensory ganglion (ganglionopathie) performs a purely sensory impairment, usually about four members without truncal root or systematization (neuropathy Sjögren’s syndrome, paraneoplastic subacute sensory neuropathy Denny-Brown, cisplatin neuropathy). There is usually an abolition or reduction of reflexes.
The radiculopathy is characterized by radicular pain, spinal starting point and radiating along the root path in question.
She is happy to cough and impulsive awakened by stretching (Lasegue in sciatic root). It may be accompanied in the territory concerned of a sensorimotor deficit systematized and the abolition of a deep tendon reflex depending on the root cause. Rarely pain is absent and it is the topography of sensory-motor deficit moving towards the root cause. The causes most frequently involved are the herniated disc, some benign tumors (neuroma, meningioma), the original neoplastic infiltration and some infections (shingles, borreliosis).
Achieving lumbosacral pluriradiculaire carries a cauda equina syndrome: flaccid sensorimotor deficit areflexic in the territory of the lumbosacral roots, saddle anesthesia, sphincter disorders.
The plexus lesions are characterized by impairment pluriradiculaire, sensorimotor, areflexic, painful or not. The causes are varied: more common for traumatic brachial plexus (dislocated shoulder), compressive (lé challenge syndrome thoracic outlet) for obstetric lumbar plexus, neoplastic (breast tumor, lung tumor apex , pelvic tumor) postradique, immunoallergic (Parsonage and Turner syndrome) or metabolic (diabetic proximal atrophy of the lower limbs).
Single vessel lesions:
The single vessel lesions cause sensorimotor reflex reached and possibly in the territory concerned, downstream of the lesion is most often focal. The causes are essentially local: trauma or compression. Achievement of the radial nerve in the arm by humerus fracture or compression during sleep, reached the ulnar at the elbow, the median carpal tunnel, the fémorocutané to the anterior superior iliac spine, the peroneal neck or fibula still Tibial the popliteal fossa.
Multivessel lesions or multiple mononeuropathies:
Multivessel mononeuropathies or multiple lesions. The mononeuropathies multiple or mononeuritis correspond to the simultaneous achievement of several nerve trunks. A frankly asymmetric distal peripheral damage can often be equated to mononeuritis.
They may be the result of vasculitis (polyarteritis nodosa, Churg-Strauss disease, Wegener’s disease, rheumatoid arthritis, lupus, cryoglobulinemia, vasculitis paraneoplastic) or diabetes and are then often painful, multifocal neuropathy conduction blocks or a tomacular neuropathy.
Polyneuropathies are characterized by bilateral and symmetrical involvement of members that can not be analyzed in terms of trunk or roots.
The distal polyneuropaties realize a distal symmetrical bilateral involvement often sensitivomotices sometimes vegetative participation. The predominant involvement of small fibers preferentially alters sensitivity and respect thermoalgique relatively proprioception and pallesthésie. The driving force and tendon reflexes may be relatively spared time. Such dissociation may occur in diabetes, amylose, leprosy, in some forms of hereditary sensory neuropathy and more incidentally in alcohol-deficiency neuropathies. The predominant involvement of large myelinated fibers preferentially altered proprioception and pallesthésie and respects the relatively thermoalgique sensitivity.
The consequenses are ataxia, paresthesias, an early abolition of tendon reflexes. The causes are the dysglobulinémies the pararanéoplasique syndromes, some toxic.
The polyradiculoneuritis realize bilateral involvement symmetrical sensorimotor usually touching the tip and root members, abolishing early and diffuse deep tendon reflexes, and accompanying himself on a lumbar puncture albumino-cytological dissociation. Acute forms correspond to Guillain-Barre syndrome, chronic forms may be secondary to hematological malignancies, an inflammatory disease or remain idiopathic.
MOTOR DEFICIT OF ORIGIN myogenic AND ACHIEVEMENT OF NEURO-MUSCULAR JUNCTION:
Motor disorders associated with impaired neuromuscular junction:
Motor disorders associated with impaired neuromuscular junction are essentially the result of myasthenia gravis that makes a postsynaptic block. It causes paralysis to the effort or aggravated by stress, affecting preferentially symmetrically roots members and dependents muscles cranial nerves (ptosis, diplopia, facial diplegia, difficulty chewing and swallowing). Diagnosis is based on the test prostigmine, electromyography, and the search for antireceptor antibodies to acetylcholine.
The risk is respiratory muscle.
Motor disorders associated with myopathy:
Movement disorders associated with myopathy combine a pure motor deficit more often proximal and symmetrical atrophy often a muscular hypertrophy, idiomusculaires abolition of reflexes, erratic conservation of deep tendon reflexes.
Rapid, sometimes general or cutaneous signs moving towards an inflammatory origin (polymyositis, dermatomyositis).
A more chronic course, family history moving towards a myopathy, a myotonic phenomenon to a Steinert disease.