The spinal cord is made up of as many segments as there are vertebral bodies.
For this reason the spinal nerves and their roots, from the cervical to the
lumbar spine, run more and more obliquely downwards.
Basically it is as if the brain, "central" signal station, through "electrical
wires", the nerves, connected itself to the periphery, like a kind of desktop
computer that is connected to keyboards, printers, modems, mice and so on.
Street.
It is clear that we can have "central" lesions, ie mainly in the brain and
surrounding structures, or "peripheral" lesions affecting the nerves starting
from the medulla. Therefore the height of the lesion is essential to know what
the consequences will be.
Let's take a practical example: if I injure my spine, I could also have injuries
to the nerves that supply the leg muscles, if the lesion is lower, but if it is
higher, even between C1 and C8, see l image, then my arms won't move either.
But it is not so simple: in fact the medulla has different structures, the
anterior and posterior horns and the lateral portions. In case of injury, if the
posterior horns are affected, the lesion will affect the motor neurons of
movement or motors, while the anterior horns contain nerve structures
responsible for sensitivity, which is why the spinal syndromes are disparate.
If any portion of the CNS is dissected, it is first noted that there are
well-defined territories in relation to each other, respectively the gray matter
and the white matter.
The gray matter mainly contains nerve cell bodies, while the white matter is composed of axons and their coatings.
In the center of the spinal cord there is a very thin central canal which is an embryonic remnant and is not infrequently occluded or dilated in a cyst. The term gray matter derives from the gray coloration of brain, medullary and ganglion cell clusters.
In transverse section it has a shape reminiscent of a butterfly: the two & quot; wings anterior i & quot; or anterior horns or, from the three-dimensional point of view, columns anterior , are relatively squat and are entirely surrounded by white matter; the hind wings or hind horns or dorsal columns, which are thinner, extend up to the limits of the spinal cord, i.e. up to the entrance of the posterior roots, where the nerve fibers arrive which collect the information of the sensitivity of the skin and mucous membranes and transmit the sensations of touch , pressure, temperature, vibration and pain , which constitutes the so-called exteroceptive sensitivity. When the spinal cord is incompletely injured in a patient, there is a partial loss of motor and sensory functions.
Most incomplete spinal cord injuries fall into place in one of the syndromes described below.
The anterior medullary syndrome. It arises from a flexion injury, due to motor paralysis and loss of pain and heat sensation below the level of the injury. Touch, proprioceptive and vibratory sensitivity are usually preserved.
The Posterior medullary syndrome produced by a hyperextension cervical injury causes only a loss of proprioception and fine tactile sensation. In fact, the posterior roots of the medulla carry the signals of sensitivity while the motor function remains intact, as it is a function of the anterior horns of the medulla and of the anterior roots of the spinal cord.
Central Medullary Syndrome is caused by a hyperextension or flexion injury. The motor deficit is variable and is greater in the arms than in the legs; the sensory damage is generally mild.
Brown-Séquard syndrome can result from a flexion, rotation, or penetration injury. The disease is characterized by unilateral ipsilateral motor paralysis and loss of pain and heat sensation contralateral to the trauma.
We can consider the following causes, associated with paralysis following central motor neuron injury.
A cerebrovascular accident involving the cortex movement can cause contralateral paresis or paralysis, onset can be sudden or gradual and the paralysis can be transient or permanent. Associated signs and symptoms vary widely and can include headache, vomiting , convulsions , decrease in the level of consciousness and cognitive functions, dysarthria, dysphagia , ataxia, paraesthesia or loss of sensation contralateral, apraxia, agnosia, aphasia , visual disturbances.
Hysterical paralysis, a classic symptom of conversion disorder, it is characterized by the loss of voluntary motility without obvious physical causes. It can affect any muscle group, appears and disappears unpredictably, and can occur with a histrionic attitude (manipulative, dramatic, afinalistic, irrational).
In the later stages of this pathology, variable paralysis develops. Earlier signs and symptoms include a rapid decrease in level of consciousness (sometimes coma ), fever , headache , photophobia, vomiting , signs of meningeal irritation (nuchal rigidity, positivity of Kernig's and Brudzinski's sign), aphasia , ataxia, nystagmus, ocular paralysis, myoclonus and convulsions .
We can consider the following conditions specified below.
Bell's palsy (see also diabetic neuropathy ), a pathology of the VIII cranial nerve causing transient unilateral facial muscle paralysis. It can also be peripheral as well as central. Today it is known that the peak of incidence is 40 years old, with 15-30 people involved every 100,000. Paralysis, as mentioned, is idiopathic and is often called "a frigore", meaning that the inflammation affecting the nerve and its geniculate ganglion and which derives from sudden changes in temperature. In reality it seems that the cause is viral (HSV or VZV), although there is no confirmation yet. Peripheral paralysis can also be caused by parotid lesions, Guillian Barrč syndrome, Lyme disease, sarcoidosis, some vaccines and acute otitis media. In these cases, however, the anamnesis and an accurate physical examination make it easy to make a differential diagnosis. No examination is therefore necessary for the diagnosis, although it must be remembered that Bell's palsy is sometimes associated with diabetes . The affected muscles are hypotonic and lid closure is impossible. Other signs include increased lacrimation, drooling and decreased or absent corneal reflex.
Severe injury to a peripheral nerve or group of nerves causes loss of motor and sensory functions in the innervated area. The muscles become flabby and atrophic and the reflexes disappear. If the transection is not complete, paralysis it may be transitory.
Complete transection of the spinal cord results in permanent spastic paralysis below the level of the lesion. Reflexes may return after resolution of the spinal shock. A partial transection causes variable paralysis with paraesthesia.
This syndrome usually causes muscle weakness which can lead to flaccid paralysis and atrophy. Associated effects include paraesthesia, loss of vibratory sensation, inactive or absent deep tendon reflexes, neuralgia and skin changes, such as anhidrosis.
This disease can cause insidious, permanent flaccid paralysis and hyporeflexia. Sensitivity remains intact but the patient loses voluntary muscle control.
This fatal disease causes spastic or flaccid paralysis of major muscle groups and eventually progresses to total paralysis. The involvement of the muscles respiratory and brain stem causes dyspnea and possibly respiratory insufficiency . Progressive cranial nerve paralysis causes dysarthria , dysphagia , sialorrhea etc.
Botulism
This bacterial toxin pathology can cause rapidly progressive weakness that progresses to paralysis within 2-4 days after ingestion of contaminated food. Human disease is caused by types A, B, E and rarely F. It is of products of the bacterium that act on the nervous system of man, of polypeptide nature and weighing 150,000 daltons. Once absorbed in the intestine or produced in an infected wound and disseminated by the systemic circulation, the toxin binds to certain receptors and blocks the transmission of acetylcholine. It follows a paralysis that mirrors the nerves involved manifesting itself as a flaccid, symmetrical and descending paralysis. Botulinum toxin is the most powerful poison for man. Type A causes strabismus and blepharospasm and dystonia. Respiratory muscular paralysis may also occur leading to dyspnea and respiratory block, nausea , vomiting , diarrhea, blurred vision or double, bilateral mydriasis, dysarthria and dysphagia are some of the earliest findings.
Advanced abscesses in the frontal or temporal lobe cause hemiplegia associated with other late findings, such as eye disorders, anisocoria, ataxia, tremors, and signs of infection.
A tumor affecting the motor cortex of the frontal lobe can cause contralateral hemiparesis that progresses to hemiplegia. Onset is gradual, but the paralysis is permanent without treatment. In the early stages, frontal headache and disorders of the behavior may be the only signs. Finally, convulsions, aphasia and signs of cerebral intracranial hypertension (decreased LDC and vomiting) appear.
This syndrome is characterized by an ascending paralysis rapidly evolving, but reversible. It usually begins with weakness in the legs and progresses symmetrically, sometimes affecting the cranial nerves, causing dysphagia, nasal voice and dysarthria.
Brain injuries can cause paralysis due to cerebral edema and increased intracranial pressure.
In this pathology neuromuscular, severe muscle weakness and abnormal fatigue can cause paralysis of some muscle groups. Paralysis is usually transient in the early stages, but becomes persistent as the disease progresses. Signs associated may include weak eye closure, ptosis, diplopia, decrease facial expression, dysphagia, nasal voice and frequent nasal regurgitation of liquids.
In the later stages of the neuro syphilis irreversible hemiplegia may occur. Dementia, paralysis of the cranial nerves, tremors and reflex abnormalities are other late findings.
Tremors, bradykinesia and hypertonic or cogwheel stiffness are the classic signs of the disease Parkinson's. Severe stiffness can progress to paralysis, especially in the limbs.
This acute illness causes progressive flaccid paralysis, vascular collapse, coma, febrile syndromes, such as cephalus, hyperesthesia, paraesthesia, cold and itching at the site of the bite, photophobia, tachycardia, shallow breathing and excessive salivation, tearing and perspiration. In 2-10 days start a phase
arousal characterized by agitation, dysfunction of the cranial nerves (pupillary changes, hoarseness, facial flaccidity) high fever, urinary retention, drooling and hydrophobia.