The clinical presentation of this disease varies with the individual as well as in severity of those symptoms. Often the symptoms include a gastrointestinal component, but many times birds suffering from this disease will present with neurologic signs as well, or in lieu of digestive anomalies.

Gastrointestinal signs may include: Regurgitation, crop impaction, poor appetite, weight loss, or passage of undigested food in the feces.

Neurologic symptoms may include: Weakness, ataxia, paresis, proprioceptive deficits, head tremors, and rarely seizures.

Muscle wasting and a generalized poor body condition is usually found as well. The virus can also affect the Purkinje cells of the heart, the adrenal medulla, the brain, and the spinal cord.

On necropsy the affected organs appear dilated and may include the crop, proventriculus, ventriculus, and small intestine. On histopathological examination the tissues will contain a lymphoplasmacytic infiltration in the peripheral and central nervous tissue. The causative virus is believed to commonly affect the myenteric plexuses which will also lead to the presentation of atrophied smooth muscle within the affected gastrointestinal organs. It is this atrophy and loss of tone in the organs that causes the dilation and subsequent gastrointestinal symptoms which are commonly the first sign of disease for the owners.

Diagnostic criteria require motor symptoms and at least one visual, sensory, or speech symptom, resembling basilar migraine. They may also be associated with cerebellar signs.

Sporadic hemiplegic migraine (SHM) is a form of hemiplegic migraine headache isolated cases of which are observed. It is a rare disease. It is considered to be a separate type of migraine.

Proventricular dilatation disease (PDD) is a disease affecting psittacines (parrots). It was first recognized and described in 1978 by Dr. Hannis L. Stoddard. Since the first reported cases were involving species of macaw, the condition was termed macaw wasting syndrome.

Caprine arthritis encephalitis (CAE) is a viral disease of goats caused by a lentivirus called caprine arthritis encephalitis virus. The disease is found worldwide.

Two syndromes of CAE occur. Adult goats develop a chronic progressive arthritis, whereas young goats develop a neurological syndrome, with signs of paresis or paralysis. Less commonly, mastitis or pneumonia may occur.

Infection is life-long, and it may be years before signs of the disease occur. The reason for the long (and variable) period of dormancy of the virus is not known.

In goats which develop arthritis, the joints become inflamed and swollen, and the goats will slowly lose condition. In some cases the goat will not be able to stand.

In goats which develop the neurological form of the disease, the onset of signs is gradual over several weeks. The hind legs are most often affected. The goat will be uncoordinated, and unable to place its feet properly, so that it "knuckles", that is, it stands with the front of its fetlock on the ground, rather than its hoof. The goat has increased difficulty standing and eventually is unable to stand.

The disease is spread to goat kids when they drink colostrum or milk from infected goats. Separating goat kids from infected goats, and feeding the kids with cow's milk, or pasteurized goat milk, will prevent infection. The disease can be spread from goat to goat via direct contact and body fluids, such as saliva. Blood testing goats for CAE virus before moving them into a new herd will prevent the spread of the disease.

There is no known cure. To prevent spread of the disease, infected animals are separated from non-infected goats, or culled.

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.

In rabbits of the genus "Sylvilagus" (cottontail rabbits) living in the Americas, myxomatosis causes only localized skin tumors, but the European rabbit ("Oryctolagus cuniculus") is more severely affected. At first, normally the disease is visible by lumps (myxomata) and puffiness around the head and genitals. It may progress to acute conjunctivitis and possibly blindness; however, this also may be the first visible symptom of the disease. The rabbits become listless, lose appetite, and develop a fever. Secondary bacterial infections occur in most cases, which cause pneumonia and purulent inflammation of the lungs. In cases where the rabbit has little or no resistance, death may take place rapidly, often in as little as 48 hours; most cases result in death within 14 days. Often the symptoms like blindness make the infected rabbit more vulnerable to predators.

Symptoms of this syndrome are consequences of this paresis. As such, in an affected patient, you may find:

- dysphonia/hoarseness

- soft palate dropping

- deviation of the uvula towards the normal side

- dysphagia

- loss of sensory function from the posterior 1/3 of the tongue

- decrease in the parotid gland secretion

- loss of gag reflex

- sternocleidomastoid and trapezius muscles paresis

Symptoms of the disease first appear from 10 to 30 years after infection. Incipient GPI is usually manifested by neurasthenic difficulties, such as fatigue, headaches, insomnia, dizziness, etc. As the disease progresses, mental deterioration and personality changes occur. Typical symptoms include loss of social inhibitions, asocial behavior, gradual impairment of judgment, concentration and short-term memory, euphoria, mania, depression, or apathy. Subtle shivering, minor defects in speech and Argyll Robertson pupil may become noticeable.

Delusions, common as the illness progresses, tend to be poorly systematized and absurd. They can be grandiose, melancholic, or paranoid. These delusions include ideas of great wealth, immortality, thousands of lovers, unfathomable power, apocalypsis, nihilism, self-blame, or bizarre hypochondriacal complaints. Later, the patient suffers from dysarthria, intention tremors, hyperreflexia, myoclonic jerks, confusion, seizures and severe muscular deterioration. Eventually, the paretic dies bedridden, cachectic and completely disoriented, frequently in a state of status epilepticus.

Neurosyphilis has four different forms: asymptomatic, meningovascular, tabes dorsalis, and general paresis. In rare instances, active neurosyphilis can mimic Alzheimer's disease.

Symptoms of neurosyphilis include, but are not limited to the following:

- Abnormal gait

- Blindness

- Confusion, disorientation

- Sudden personality changes

- Changes in mental stability

- Dementia

- Depression

- Headache

- Fecal and urinary incontinence

- Irritability

- Memory problems

- Mood disturbances

- Numbness in the toes, feet, or legs

- Poor concentration

- Psychosis

- Seizures

- Neck stiffness

- Tremors

- Visual disturbances. There may be the sign of Argyll Robertson pupils, which are bilateral small pupils that constrict when the patient focuses on a near object but do not constrict when exposed to bright light.

- Muscle weakness

Upon further diagnostic workup, the following signs may be present:

- Abnormal reflexes

- Muscle atrophy

- Muscle contractions

The diagnosis could be differentiated from other known psychoses and dementias by a characteristic abnormality in eye pupil reflexes (Argyll Robertson pupil), and, eventually, the development of muscular reflex abnormalities, seizures, memory impairment (dementia) and other signs of relatively pervasive neurocerebral deterioration. Definitive diagnosis is based on the analysis of cerebrospinal fluid and tests for syphilis.

The defining characteristic of BPT is a tilting of an infant’s head in recurrent episodes, for varying periods of time. Furthermore, the child’s trunk may bend in the same direction as the head, giving the baby an overall curved shape; this complaint is known as tortipelvis. In addition to this, the individual may also, but not necessarily, experience vomiting, pallor, ataxia, agitation, infantile migraine, unsteadiness of gait upon learning to walk, general malaise and nystagmus.

The periods in which the child’s head is tilted and other symptoms appear can last anywhere from a few minutes to a few weeks, with a frequency of anywhere from two per year to two per month.

Myxomatosis (sometimes shortened to "myxo" or "myxy") is a disease that affects rabbits, caused by the "myxoma" virus. It was first observed in Uruguay in laboratory rabbits in the late 19th century. It was introduced into Australia in 1950 in an attempt to control the rabbit population (see Rabbits in Australia). Affected rabbits develop skin tumors, and in some cases blindness, followed by fatigue and fever; they usually die within 14 days of contracting the disease.

The disease is spread by direct contact with an affected animal or by being bitten by fleas or mosquitoes that have fed on an infected rabbit. The myxomatosis virus does not replicate in these insect hosts, but can be physically carried by an insect's mouthparts, i.e. from an infected rabbit to another susceptible animal. Due to the potential of insect vector transmission, pet rabbits may be susceptible in enzootic areas and vaccination is highly recommended.

Symptoms are very similar to those found in benign fasciculation syndrome and include:

- Fasciculations (Primary Symptom)

- Muscle cramping (Primary Symptom)

- Muscle pain

- Muscle Stiffness

- Generalized fatigue

- Anxiety

- Exercise intolerance

- Globus sensations

- Paraesthesias.

- Hyperreflexia

People with ODD syndrome often have a characteristic appearance. Visible features of the condition include:

- small teeth that are prone to caries because of underdeveloped tooth enamel;

- a long, thin nose;

- unusually small eyes; and

- type III syndactyly of the fourth and fifth fingers.

Iris atrophy and glaucoma are more common than average. The size of the eyes often interferes with learning to read; special eyeglasses may be required. Hair may be fine, thin, dry, or fragile; in some families, it is curly.

Neurologic abnormalities may be seen in adults. The neurologic changes may appear earlier in each subsequent generation and can include abnormal white matter, conductive deafness, and various kinds of paresis, including ataxia, spastic paraplegia, difficulty controlling the eyes, and bladder and bowel disturbances.

The procedure of diagnosis for Cramp Fasciculation Syndrome (CFS) is closely aligned with the diagnosis procedure for benign fasciculation syndrome (BFS). The differentiation between a diagnosis of BFS versus CFS is usually more severe and prominent pain, cramps and stiffness associated with CFS.

Benign lymphoepithelial lesion is most likely to occur in adults around 50 years of age. There is a predilection for gender with 60–80% being female. The gland affected has a diffuse swelling. The swelling can be asymptomatic, but mild pain can also be associated. There is a preponderance of this disease in those who suffer from HIV infection.

Most cases of benign lymphoepithelial lesions appear in conjunction with Sjögren's syndrome. When Sjögren's syndrome is present, the swelling is usually bilateral. Otherwise, the affected glands are usually only on one side of the body.

In many cases, a biopsy is needed to distinguish benign lymphoepithelial lesions from sialadenosis (sialosis).

Benign paroxysmal torticollis (BPT) is a rare medical disorder affecting infants.

Cobb syndrome is a rare congenital disorder characterized by visible skin lesions with underlying spinal angiomas or arteriovenous malformations (AVMs). The skin lesions of Cobb syndrome typically are present as port wine stains or angiomas, but reports exist of angiokeratomas, angiolipomas, and lymphangioma circumscriptum. The intraspinal lesions may be angiomas or AVMs and occur at levels of the spinal cord corresponding to the affected skin dermatomes. They may in turn produce spinal cord dysfunction and weakness or paralysis.

The disorder was first described by Berenbruch in 1890, but became widely known only after Cobb's report in 1915. Cobb syndrome is thought to be more common in males and have no racial predilection, but only a few dozen cases are known. It is believed to be due to a sporadic mutation, since parents of affected children usually have no evidence of the disease.

Historically, bilateral parotid and lacrimal gland enlargement was characterized by the term Mikulicz's disease if the enlargement appeared apart from other diseases. If it was secondary to another disease, such as tuberculosis, sarcoidosis, lymphoma, and Sjögren's syndrome, the term used was Mikulicz's syndrome. Both names derive from Jan Mikulicz-Radecki, the Polish surgeon best known for describing these conditions.

In more recent times, the terms "Mikulicz's disease" and "Mikulicz's syndrome" were viewed as ambiguous and outdated by some sources.

Today Mikulicz's disease is considered to be a subtype of IgG4-related disease, usually accompanied by involvement of one or more other organs in the body.

Postoperative residual curarization (PORC) is a residual paresis after emergence from general anesthesia with neuromuscular-blocking drugs.

VBD

- Hemifacial spasm

- Paresis

- Trigeminal neuralgia

ICD

- Progressive visual field defect

Worster-Drought syndrome is a form of congenital suprabulbar paresis that occurs in some children with cerebral palsy. It is caused by inadequate development of the corticobulbar tracts and causes problems with the mouth and tongue including impaired swallowing. A similar syndrome in adults is called anterior opercular syndrome.

A 1986 study of a family in which multiple members had Worster-Drought Syndrome suggested it might be hereditary.

A 2000 review of cases classified Worster-Drought Syndrome as a form of cerebral palsy, caused by early damage to the brain, but identified no obvious causes during gestation or birth and found some families with a history of the condition.

The syndrome was named after Cecil Charles Worster-Drought, the doctor who discovered it in 1956.

Voice disorders are medical conditions involving abnormal pitch, loudness or quality of the sound produced by the larynx and thereby affecting speech production. These include:

- Puberphonia

- Chorditis

- Vocal fold nodules

- Vocal fold cysts

- Vocal cord paresis

- Reinke's edema

- Spasmodic dysphonia

- Foreign accent syndrome

- Bogart–Bacall syndrome

- Laryngeal papillomatosis

- Laryngitis

Jugular foramen syndrome, or Vernet's syndrome is characterized by the paresis of 9th–11th (with or without 12th) cranial nerves together.