Tetraparesis is defined as reduced voluntary motor function in all four limbs, and can be subdivided into ambulatory and non-ambulatory categories.
Tetraplegia indicates total absence of voluntary motor function in all four limbs.
Tetraparesis can result from focal diseases of the brainstem and spinal cord, or generalized diseases of the peripheral nervous system (PNS), including diseases of the neuromuscular junction and muscle. It can also be caused by non-neurological diseases (). A careful physical and neurological examination is therefore needed to localize the source of weakness.
Non-neurological diseases that can cause tetraparesis:
- Polymyositis ()
- Hypertrophic osteodystrophy
In tetraparetic animals the pelvic limbs are often affected earlier and more severely than the thoracic limbs, and severity of signs can range from mild weakness and ataxia to tetraplegia with respiratory failure.
Tetraplegic animals are at serious risk of respiratory failure due to paresis of the intercostal muscles and diaphragm, atelectasis as a result of recumbency, aspiration pneumonia, or failure of respiratory drive (if the brainstem is involved).
Animals with central nervous system (CNS) causes of tetraparesis are ataxic and have conscious proprioceptive and postural reaction deficits in ail four limbs. Neck pain may be present, depending on the aetiology of signs and the individual (). Myotatic reflexes and muscle tone in the pelvic limbs are normal to increased; in the thoracic limbs they may be normal to increased, or decreased, depending on the neurolocalization (C1-5 and C6-T2, respectively). Caudal cervical lesions can cause: lameness in one or both thoracic limbs; a short, stilted thoracic limb gait; muscle atrophy of the supra- and infraspinatous and biceps brachii muscles; and at rest animals may hold the affected limb(s) off the ground. These signs are a result of compression of nerve roots causing pain and weakness (nerve root signature). Lateralized cervical spinal cord lesions can produce partial Homer’s syndrome (miosis) on the affected side as a result of involvement of the sympathetic fibres running in the lateral funiculus of the spinal cord and emerging from the spinal cord at segments T1 -3. Lesions affecting spinal cord segments C8-T2 can affect the motor (effector) arm of the cutaneous trunci reflex, the lateral thoracic nerve, causing complete loss of the reflex on the affected side. In addition to tetraparesis, brainstem involvement causes cranial nerve deficits, in particular vestibular dysfunction, and can cause changes in mentation. In both brainstem and spinal cord disease, lateralized lesions produce ipsilateral deficits (e.g. hemiparesis).
Generalized lower motor neuron (LMN) diseases cause weakness characterized by decreased muscle tone (flaccidity) and decreased or absent myotatic reflexes. Ataxia and postural reaction and conscious pro-prioceptive deficits may also be present. Involvement of the recurrent laryngeal nerve can cause a change in, or loss of, voice (dysphonia) and increased inspirator / noise (stridor). The development of megaoesophagus can cause regurgitation, often with accompanying aspiration pneumonia, particularly if the pharyngeal and laryngeal muscles are concurrently involved. Other cranial nerve deficits such as facial paresis may be present. As disease progresses, dramatic muscle atrophy develops; although muscle hypertrophy occurs in some myopathies and peripheral neuropathies. Myopathies can usually be distinguished from neuropathies as myotatic reflexes are usually normal and there are no conscious proprioceptive deficits. However, adequate support must be given to very weak animals in order to test conscious proprioception accurately. Exercise intolerance can be the only sign present in some myopathies and disorders of neuromuscular transmission, such as myasthenia gravis. ()
Any animal that is tetraplegic, whether the cause is spinal or peripheral in origin, is at risk from hypoventilation and so an arterial blood gas analysis should be performed to measure the partial pressure of carbon dioxide. Ventilatory support by means of a mechanical ventilator may be necessary in animals with an arterial partial pressure of CO2 of >50-60 mmHg. In small animals (<5 kg) a transtracheal catheter can be used in place of a ventilator. The catheter is advanced via the cricothyroid ligament to the level of the bronchial bifurcation, and a humidified oxygen / air mixture is passed through the catheter at a rate sufficient to exchange carbon dioxide adequately. Any animal with regurgitation is at risk of developing aspiration pneumonia: the lung fields should be auscultated carefully, and thoracic radiographs and an arterial blood gas analysis performed if there is any suspicion of aspiration.
Non-neurological causes of tetraparesis should be suspected whenever conscious proprioception is normal. Careful palpation of joints and long bones will enable the clinician to identify orthopaedic diseases such as polyarthritis and hypertrophic osteodystrophy.
Tetraparesis can result from:
- Focal lesions in the cervical spinal cord or brainstem
- Diffuse spinal cord diseases
- Generalized diseases of the peripheral nerve, neuromuscular junction and muscle.
Conduction of nerve impulses is dependent on the integrity of the neuronal cell body, the axon, the myelin sheath and the junction between a neuron and its target. Neurons have excitable membranes due to selective ionic permeability. In the resting state, the membrane is polarized to a potential of approximately -70mV as a result of partial permeability to potassium and active extrusion of sodium in exchange for potassium.
Action potentials are generated by rapid influx of sodium through voltage-dependent channels that are opened by depolarization of the membrane. This membrane depolarization results from the activation of receptors by neurotransmitters: either excitatory (causing membrane depolarization) or inhibitory (causing membrane hyperpolarization) (). The membrane is repolarized by closure of the sodium channels (halting the influx of sodium) and opening of voltage-dependent potassium channels (producing efflux of potassium). Action potentials that conduct down the axon are triggered at the axon hillock (the junction between the axon and neuronal cell body).
Speed of conduction is largely dependent on axon diameter (larger diameter conducts more quickly) and myelination. Myelin, produced by oligodendrocytes in the CNS and Schwann cells in the PNS, insulates axons, increasing their membrane resistance (). This causes conduction of action potentials in a simple cable fashion to the next region of exposed axon membrane (node), where depolarization of the membrane produces a new action potential. The result is conduction of the impulse from node to node in a saltatory fashion, dramatically increasing the speed of conduction.
Spinal cord dysfunction most commonly results from compression, concussion, laceration, ischaemia or inflammation, with many diseases producing a combination of these problems. Less commonly, neurodegenerative and toxic disorders can affect the spinal cord. Neurons within the CNS cannot regenerate axons and so recovery following axonal transection or neuronal death depends on the development of alternative routes of conduction using surviving tissue. As a result, prognosis in spinal cord disease, no matter what the aetiology, is greatly influenced by the severity of damage at the time of evaluation.
Treatment of spinal cord diseases focuses on surgical decompression of compressive lesions, appropriate treatment of infectious and inflammatory diseases and physical therapy to facilitate and maximize recovery.
Neurons in the peripheral nervous system are more resistant to injury than their CNS counterparts and are able to regenerate axons at a surprising speed (1-4 mm / day) if they are regenerating within an intact endoneural and Schwann cell tube. However, when a nerve is completely severed and displaced (neurotmesis), successful regeneration to a target only occurs if the axon is able to find the distal stump of the nerve.
Although the same basic injury types apply to peripheral nerves, metabolic, inherited and toxic disorders assume a greater clinical importance than in the spinal cord. In most peripheral neuropathies a mixture of demyelination and axonal degeneration is present. The distal ends of axons are particularly susceptible to degeneration as a result of their distance from the neuronal cell body, with longer nerves (recurrent laryngeal and sciatic nerves) often clinically affected first in toxic, degenerative and metabolic disorders.
The history and findings of the physical and neurological examinations will allow identification of a neurological problem and localization to brainstem, spinal cord or PNS. Diagnostic evaluation of animals with evidence of spinal cord disease starts with routine blood work (complete blood cell count, serum biochemical analysis and urinalysis) and survey spinal radiographs. Survey thoracic radiographs should be taken in any animal in which neoplasia is a differential, to identify metastatic disease. As a general rule, if a diagnosis cannot be reached from survey radiographs, the animal should be referred to a specialist centre for further evaluation, including advanced imaging.
Minimum diagnostic work-up for dogs with generalized LMN signs includes a complete blood cell count, serum biochemical panel including creatine kinase (CK), urinalysis, and chest radiographs to identify megaoesophagus, aspiration pneumonia and pulmonary metastases. Although nerve and muscle biopsies may provide a definitive diagnosis, further testing is often needed based on biopsy results ().
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