A medical condition, Locked-in syndrome usually resulting from a stroke that damages part of the brainstem, in which the body and most of the facial muscles are paralysed but consciousness remains and the ability to perform certain eye movements is preserved.

Parkinson's disease, or PD, is a progressive illness of the nervous system. Caused by the death of dopamine-producing brain cells that affect motor skills and speech. Symptoms may include bradykinesia (slow physical movement), muscle rigidity, and tremors. Behavior, thinking, sensation disorders, and the sometimes co-morbid skin condition Seborrheic dermatitis are just some of PD's numerous nonmotor symptoms. Parkinson's disease, Attention deficit/hyperactivity disorder (ADHD) & Bi-polar disorder, all appear to have some connection to one another, as all three nervous system disorders involve lower than normal levels of the brain chemical dopamine(In ADHD, Parkinson's, & the depressive phase of Bi-polar disorder.) or too much dopamine (in Mania or Manic states of Bi-polar disorder) in different areas of the brain:

Dissociated sensory loss is a pattern of neurological damage caused by a lesion to a single tract in the spinal cord which involves "selective" loss of fine touch and proprioception "without" loss of pain and temperature, or vice versa.

Understanding the mechanisms behind these selective lesions requires a brief discussion of the anatomy involved.

Loss of pain and temperature are due to damage to the lateral spinothalamic tracts, which cross the central part of the cord close to the level where they enter it and travel up the spinal column on the opposite side to the one they innervate (i.e. they "ascend contralaterally"). Note that a lesion of the lateral spinothalamic tract at a given level will not result in sensory loss for the dermatome of the same level; this is due to the fibers of the tract of Lissauer which transmit the neuron one or two levels above the affected segment (thus bypassing the segmental lesion on the contralateral side).

Loss of fine touch and proprioception are due to damage to the dorsal columns, which do not cross the cord until the brainstem, and so travel up the column on the same side to the one they innervate (i.e. they "ascend ipsilaterally").

This means that a lesion of the dorsal columns will cause loss of touch and proprioception below the lesion and on the same side as it, while a lesion of the spinothalamic tracts will cause loss of pain and temperature below the lesion and on the opposite side to it.

Dissociated sensory loss always suggests a focal lesion within the spinal cord or brainstem.

The location of cord lesions affects presentation—for instance, a central lesion (such as that of syringomyelia) will knock out second order neurons of the spinothalamic tract as they cross the centre of the cord, and will cause loss of pain and temperature without loss of fine touch or proprioception.

Other causes of dissociated sensory loss include:

- Diabetes mellitus

- Syringomyelia

- Brown-Séquard syndrome

- Lateral medullary syndrome aka Wallenberg's syndrome

- Anterior spinal artery thrombosis

- Tangier disease

- Subacute combined degeneration

- Multiple sclerosis

- Tabes dorsalis

- Friedreich's ataxia (or other spinocerebellar degeneration)

CCS is characterized by disproportionately greater motor impairment in upper compared to lower extremities, and variable degree of sensory loss below the level of injury in combination with bladder dysfunction and urinary retention. This syndrome differs from that of a complete lesion, which is characterized by total loss of all sensation and movement below the level of the injury.

The condition usually consists of:

Sensation to the face is preserved, due to the sparing of the trigeminal nucleus.

The syndrome is said to be "alternating" because the lesion causes symptoms both contralaterally and ipsilaterally. Sensation of pain and temperature is preserved, because the spinothalamic tract is located more laterally in the brainstem and is also not supplied by the anterior spinal artery (instead supplied by the posterior inferior cerebellar arteries and the vertebral arteries).

Symptoms vary depending on whether the spinal cord, brain stem, nerves or their blood supply is affected by the pressure.

Symptoms become apparent when the neck is bent. They include:

- Posterior head pain

- Neck weakness

- Periods of confusion

- Dysarthria (difficulty swallowing or talking due to loss of muscle control)

- Dizziness

- Loss of sensation

- Cranial nerve disturbance

- Loss of the ability to know how joints are positioned

- Lhermitte's sign ('electric shock sensation' down spine and/or to the extremities when the neck is flexed forward)

- Weakness of the arms and legs

- Orthostatic hypotension

- Patients will go into a pool and notice that below their belly button the water is not as cold as it is above.

Complications from this can include hydrocephalus, pseudotumor cerebri or syringomyelia because it blocks the flow of fluid around the brain and spinal cord.

Medial medullary syndrome, also known as inferior alternating syndrome, hypoglossal alternating hemiplegia, lower alternating hemiplegia, or Dejerine syndrome, is a type of alternating hemiplegia characterized by a set of clinical features resulting from occlusion of the anterior spinal artery. This results in the infarction of medial part of the medulla oblongata.

There are disturbances in sensory nerves and motor nerves and dysfunction of the autonomic nervous system at the level of the lesion or below. Therefore, the signs and symptoms depend on the area of spine involved:

- Cervical: If the upper cervical cord is involved, all four limbs may be involved and there is risk of respiratory paralysis (cervical nerve segments C3, 4, 5 innervate the abdominal diaphragm). Lesions of the lower cervical (C5–T1) region will cause a combination of upper and lower motor neuron signs in the upper limbs, and exclusively upper motor neuron signs in the lower limbs. Cervical lesions account for about 20% of cases.

- Thoracic: A lesion of the thoracic spinal cord (T1–12) will produce upper motor neuron signs in the lower limbs, presenting as a spastic diplegia. This is the most common location of the lesion,

The disease is present at birth, but clinical manifestations are often not seen until later in life. Patients typically experience the sudden onset of pain, numbness, or weakness in their extremities as children or young adults. These symptoms may remit or remain stable and often can be localized below a specific dermatome. Symptoms tend to worsen over time either by discrete steps or continuously. Early development of weakness may portend a more aggressive course. Less commonly, weakness or bowel and bladder dysfunction may be presenting symptoms.

The major debility from Cobb syndrome is the onset of weakness, paresis, sensory loss, and loss of bowel and bladder control. A possible complication if treatment is delayed is Foix-Alajouanine disease or subacute necrotic myelopathy due to thrombosis in the spinal angioma.

Cutaneous lesions may be distributed anywhere in the dermatome, from midline back to abdomen. Midline back lesions may be associated with spina bifida. The cutaneous lesion may be very faint and may be more pronounced when the patient performs a Valsalva maneuver which increases abdominal pressure and causes preferential filling of the cutaneous angioma. Neurological examination will reveal weakness or paralysis and numbness or decreased sensation with a sharp upper cutoff.

Clinical signs and symptoms depend on which spinal cord level (cervical, thoracic or lumbar) is affected and the extent (anterior, posterior or lateral) of the pathology, and may include:

- upper motor neuron signs—weakness, spasticity, clumsiness, altered tonus, hyperreflexia and pathological reflexes, including Hoffmann's sign and inverted Plantar reflex (positive Babinski sign);

- lower motor neuron signs—weakness, clumsiness in the muscle group innervated at the level of spinal cord compromise, muscle atrophy, hyporeflexia, muscle hypotonicity or flaccidity, fasciculations;

- sensory deficits;

- bowel/bladder symptoms and sexual dysfunction.

Changes in muscle performance can be broadly described as the upper motor neuron syndrome. These changes vary depending on the site and the extent of the lesion, and may include:

- Muscle weakness. A pattern of weakness in the extensors (upper limbs) or flexors (lower limbs), is known as 'pyramidal weakness'

- Decreased control of active movement, particularly slowness

- Spasticity, a velocity-dependent change in muscle tone

- Clasp-knife response where initial higher resistance to movement is followed by a lesser resistance

- Babinski sign is present, where the big toe is raised (extended) rather than curled downwards (flexed) upon appropriate stimulation of the sole of the foot. The presence of the Babinski sign is an abnormal response in adulthood. Normally, during the plantar reflex, it causes plantar flexion and the adduction of the toes. In Babinski's sign, there is dorsiflexion of the big toe and abduction of the other toes. Physiologically, it is normally present in infants from birth to 12 months. The presence of the Babinski sign after 12 months is the sign of a non-specific upper motor neuron lesion.

- Increased deep tendon reflex (DTR)

- Pronator drift

Spinal shock was first defined by Whytt in 1750 as a loss of accompanied by motor paralysis with initial loss but gradual recovery of reflexes, following a spinal cord injury (SCI) – most often a complete transection. Reflexes in the spinal cord below the level of injury are depressed (hyporeflexia) or absent (areflexia), while those above the level of the injury remain unaffected. The 'shock' in spinal shock does not refer to circulatory collapse, and should not be confused with neurogenic shock, which is life-threatening

In spinal cord injuries above T6, neurogenic shock may occur, from the loss of autonomic innervation from the brain. Parasympathetic is preserved but the synergy between sympathetic and parasympathetic system is lost in cervical and high thoracic SCI lesions. Sacral parasympathetic loss may be encountered in lesions below T6 or T7. Cervical lesions cause total loss of sympathetic innervation and lead to vasovagal hypotension and bradyarrhythmias – which resolve in 3–6 weeks. Autonomic dysreflexia is permanent, and occurs from Phase 4 onwards. It is characterized by unchecked sympathetic stimulation below the SCI (from a loss of cranial regulation), leading to often extreme hypertension, loss of bladder or bowel control, sweating, headaches, and other sympathetic effects.

Syringomyelia causes a wide variety of neuropathic symptoms due to damage of the spinal cord and the nerves inside. Patients may experience severe chronic pain, abnormal sensations and loss of sensation particularly in the hands. Some patients experience paralysis or paresis temporarily or permanently. A syrinx may also cause disruptions in the parasympathetic and sympathetic nervous systems, leading to abnormal body temperature or sweating, bowel control issues, or other problems. If the syrinx is higher up in the spinal cord or affecting the brainstem as in syringobulbia, vocal cord paralysis, ipsilateral tongue wasting, trigeminal nerve sensory loss, and other signs may occur. Rarely, bladder stones can occur in the onset of weakness in the lower extremities.

Classically, syringomyelia spares the dorsal column/medial lemniscus of the spinal cord, leaving pressure, vibration, touch and proprioception intact in the upper extremities. Neuropathic arthropathy, also known as a Charcot joint, can occur, particularly in the shoulders, in patients with syringomyelia. The loss of sensory fibers to the joint is theorized to lead to damage of the joint over time.

Paraplegia is an impairment in motor or sensory function of the lower extremities. The word comes from Ionic Greek παραπληγίη "half-striking". It is usually caused by spinal cord injury or a congenital condition that affects the neural (brain) elements of the spinal canal. The area of the spinal canal that is affected in paraplegia is either the thoracic, lumbar, or sacral regions. Common victims of this impairment are veterans or members of the armed forces. If four limbs are affected by paralysis, tetraplegia or quadriplegia is the correct term. If only one limb is affected, the correct term is monoplegia.

Spastic paraplegia is a form of paraplegia defined by spasticity of the affected muscles, rather than flaccid paralysis.

The American Spinal Injury Association classifies spinal cord injury severity. ASIA A being the complete loss of sensory function and motor skills below the injury. ASIA B is having some sensory function below the injury, but no motor function. ASIA C some motor function below level of injury, but half the muscles cannot move against gravity. ASIA D, more than half of the muscles below the level of injury can move against gravity. ASIA E which is the restoration of all neurologic function.

The onset of myelomalacia may be so subtle that it is overlooked. Depending on the extent of the spinal cord injury, the symptoms may vary. In some cases, the symptom may be as common as hypertension. Though every case is different, several cases reported loss of motor functions in the extremities, areflexia or sudden jerks of the limbs, loss of pain perception, or even paralysis; all of which are possible indicators of a damaged and softened spinal cord. In the most severe cases, paralysis of the respiratory system manifests in death.

In older patients, CCS most often occurs after acute hyperextension injury in an individual with long-standing cervical spondylosis. A slow, chronic cause in this age group is when the cord gets caught and squeezed between a posterior intervertebral disc herniation against the anterior cord and/or with posterior pressure on the cord from hypertrophy of the ligamentum flavum (Lhermitte's sign may be the experience that causes the patient to seek medical diagnosis). However, CCS is not exclusive to older patients as younger individuals can also sustain an injury leading to CCS. Typically, younger patients are more likely to get CCS as a result of a high-force trauma or a bony instability in the cervical spine. Historically, spinal cord damage was believed to originate from concussion or contusion of the cord with stasis of axoplasmic flow, causing edematous injury rather than destructive hematomyelia. More recently, autopsy studies have demonstrated that CCS may be caused by bleeding into the central part of the cord, portending less favorable prognosis. Studies also have shown from postmortem evaluation that CCS probably is associated with selective axonal disruption in the lateral columns at the level of the injury to the spinal cord with relative preservation of the grey matter.

For the ossificans form of the condition, unenhanced CT may better show the presence and extent of arachnoid ossifications, and is complementary to MRI, as MRI can be less specific and findings can be confused with regions of calcification or hemosiderin.

Brown-Séquard syndrome (also known as Brown-Séquard's hemiplegia, Brown-Séquard's paralysis, hemiparaplegic syndrome, hemiplegia et hemiparaplegia spinalis, or spinal hemiparaplegia) is caused by damage to one half of the spinal cord, resulting in paralysis and loss of proprioception on the same (or ipsilateral) side as the injury or lesion, and loss of pain and temperature sensation on the opposite (or contralateral) side as the lesion. It is named after physiologist Charles-Édouard Brown-Séquard, who first described the condition in 1850.

Arachnoid inflammation can lead to many painful and debilitating symptoms which can vary greatly in each case, and not all people experience all symptoms. Chronic pain is common, including neuralgia, while numbness and tingling of the extremities can occur with spinal cord involvement, and bowel, bladder, and sexual functioning can be affected if the lower part of the spinal cord is involved. While arachnoiditis has no consistent pattern of symptoms, it frequently affects the nerves that supply the legs and lower back. Many patients experience difficulty sitting for long (or even short) periods of time due to discomfort or pain, or because of efferent neurological or other motor symptoms, such as difficulties controlling limbs. Difficulty sitting can be problematic for patients who have trouble standing or walking for long periods, as wheelchairs are not always helpful in such cases.

Symptoms usually occur very quickly and are often experienced within one hour of the initial damage. MRI can detect the magnitude and location of the damage 10–15 hours after the initiation of symptoms. Diffusion-weighted imaging may be used as it is able to identify the damage within a few minutes of symptomatic onset.

Clinical features include paraparesis or quadriparesis (depending on the level of the injury) and impaired pain and temperature sensation. Complete motor paralysis below the level of the lesion due to interruption of the corticospinal tract, and loss of pain and temperature sensation at and below the level of the lesion. Proprioception and vibratory sensation is preserved, as it is in the dorsal side of the spinal cord.

This condition is distinct and usually episodic, with the people experiencing remarkably high blood pressure (often with systolic readings over 200 mm. Hg), intense headaches, profuse sweating, facial erythema, goosebumps, nasal stuffiness, a "feeling of doom" or apprehension, and blurred vision. An elevation of 40 mm Hg over baseline systolic should be suspicious for dysreflexia.

Autonomic dysreflexia can become chronic and recurrent, often in response to longstanding medical problems like soft tissue ulcers or hemorrhoids. Long term therapy may include alpha blockers or calcium channel blockers.

Complications of severe acute hypertension can include seizures, pulmonary edema, myocardial infarction or cerebral hemorrhage. Additional organs that may be affected include the kidneys and retinas of the eyes.

Basilar invagination is invagination (infolding) of the base of the skull that occurs when the top of the C2 vertebra migrates upward. It can cause narrowing of the foramen magnum (the opening in the skull where the spinal cord passes through to the brain). It also may press on the lower brainstem.

This is similar to Chiari malformation. That, however, is usually present at birth.

Brown-Séquard syndrome may be caused by a spinal cord tumour, trauma [such as a gunshot wound or puncture wound to the cervical (neck) or thoracic spine (back)], ischemia (obstruction of a blood vessel), or infectious or inflammatory diseases such as tuberculosis, or multiple sclerosis. In its pure form, it is rarely seen. The most common cause is penetrating trauma such as a gunshot wound or stab wound to the spinal cord. Decompression sickness may also be a cause of Brown-Séquard syndrome.

The presentation can be progressive and incomplete. It can advance from a typical Brown-Séquard syndrome to complete paralysis. It is not always permanent and progression or resolution depends on the severity of the original spinal cord injury and the underlying pathology that caused it in the first place.