The presenting symptom of dementia with Lewy bodies is often cognitive dysfunction, though dementia eventually occurs in all individuals with DLB. In contrast to Alzheimer's disease (AD), in which memory loss is the first symptom, those with DLB first experience impaired attention, executive function, and visuospatial function, while memory is affected later. These impairments present as driving difficulty, such as becoming lost, misjudging distances, or as impaired job performance. In terms of cognitive testing, individuals may have problems with figure copying as a result of visuospatial impairment, with clock-drawing due to executive function impairment, and difficulty with serial sevens as a result of impaired attention. Short-term memory and orientation to time and place remain intact in the earlier stages of the disease.

While the specific symptoms in a person with DLB may vary, core features include: fluctuating cognition with great variations in attention and alertness from day to day and hour to hour, recurrent visual hallucinations (observed in 75% of people with DLB), and motor features of Parkinson's disease. Suggestive symptoms are rapid eye movement (REM)-sleep behavior disorder and abnormalities detected in PET or SPECT scans. REM sleep behavior disorder (RBD) often is a symptom first recognized by the patient's caretaker. RBD includes vivid dreaming, with persistent dreams, purposeful or violent movements, and falling out of bed. Benzodiazepines, anticholinergics, surgical anesthetics, some antidepressants, and over-the-counter drug cold remedies may cause acute confusion, delusions, and hallucinations.

Tremors are less common in DLB than in Parkinson's disease. Parkinsonian features may include shuffling gait, reduced arm-swing during walking, blank expression (reduced range of facial expression), stiffness of movements, ratchet-like cogwheeling movements, low speech volume, sialorrhea, and difficulty swallowing. Also, DLB patients often experience problems with orthostatic hypotension, including repeated falls, fainting, and transient loss of consciousness. Sleep-disordered breathing, a problem in multiple system atrophy, also may be a problem.

One of the most critical and distinctive clinical features of the disease is hypersensitivity to neuroleptic and antiemetic medications that affect dopaminergic and cholinergic systems. In the worst cases, a patient treated with these medications could become catatonic, lose cognitive function, or develop life-threatening muscle rigidity. Some commonly used medications that should be used with great caution, if at all, for people with DLB, are chlorpromazine, haloperidol, or thioridazine.

Visual hallucinations in people with DLB most commonly involve perception of people or animals that are not there, and may reflect Lewy bodies or AD pathology in the temporal lobe. Delusions may include reduplicative paramnesia and other elaborate misperceptions or misinterpretations. These hallucinations are not necessarily disturbing, and in some cases, the person with DLB may have insight into the hallucinations and even be amused by them, or be conscious they are not real. People with DLB also may have problems with vision, including double vision, and misinterpretation of what they see, for example, mistaking a pile of socks for snakes or a clothes closet for the bathroom.

Some of the most prevalent symptom types in people exhibiting CBD pertain to identifiable movement disorders and problems with cortical processing. These symptoms are initial indicators of the presence of the disease. Each of the associated movement complications typically appear asymmetrically and the symptoms are not observed uniformly throughout the body. For example, a person exhibiting an alien hand syndrome (explained later) in one hand, will not correspondingly display the same symptom in the contralateral limb. Predominant movement disorders and cortical dysfunctions associated with CBD include:

- Parkinsonism

- Alien hand syndrome

- Apraxia (ideomotor apraxia and limb-kinetic apraxia)

- Aphasia

The presence of parkinsonism as a clinical symptom of CBD is largely responsible for complications in developing unique diagnostic criteria for the disease. Other such diseases in which parkinsonism forms an integral diagnostic characteristic are PD and PSP. Parkinsonism in CBD is largely present in an extremity such as the arm, and is always asymmetric. It has been suggested that non-dominant arm is involved more often. Common associated movement dysfunctions that comprise parkinsonism are rigidity, bradykinesia, and gait disorder, with limb rigidity forming the most typical manifestation of parkinsonism in CBD. Despite being relatively indistinct, this rigidity can lead to disturbances in gait and correlated movements. Bradykinesia in CBD occurs when there is notable slowing in the completion of certain movements in the limbs. In an associated study, it was determined that, three years following first diagnosis, 71% of persons with CBD demonstrate the presence of bradykinesia.

Differentiating some kinds of atypical Parkinson: Northwest Parkinson Foundation

Before Parkinson's disease is diagnosed, the differential diagnoses include:

- AIDS can sometimes lead to the symptoms of secondary parkinsonism, due to commonly causing dopaminergic dysfunction. Indeed, parkinsonism can be a presenting feature of HIV infection.

- Corticobasal degeneration

- Creutzfeldt–Jakob disease

- Dementia pugilistica or "boxer's dementia" is a condition that occurs in athletes due to chronic brain trauma.

- Diffuse Lewy body disease

- Drug-induced parkinsonism ("pseudoparkinsonism") due to drugs such as antipsychotics, metoclopramide, sertraline, fluoxetine or the toxin MPTP

- Encephalitis lethargica

- Essential tremor, an illness which has some diagnostic overlap with Parkinson's disease

- Orthostatic tremor

- MDMA addiction and frequent use has been linked to Parkonsonism. Several cases have been reported where individuals are diagnosed with the syndrome after taking MDMA.

- Multiple system atrophy

- Pantothenate kinase-associated neurodegeneration, also known as neurodegeneration with brain iron accumulation or Hallervorden-Spatz syndrome

- Parkinson plus syndrome

- Progressive supranuclear palsy

- Toxicity due to substances such as carbon monoxide, carbon disulfide, manganese, paraquat, mercury, hexane, rotenone, Annonaceae, and toluene (inhalant abuse: "huffing")

- Vascular parkinsonism, associated with underlying cerebrovascular disease

- Wilson's disease is a genetic disorder in which an abnormal accumulation of copper occurs. The excess copper can lead to the formation of a copper-dopamine complex, which leads to the oxidation of dopamine to aminochrome. The most common manifestations include bradykinesia, cogwheel rigidity and a lack of balance.

- Paraneoplastic syndrome: neurological symptoms caused by antibodies associated with cancers

- Genetic

- Rapid onset dystonia parkinsonism

- Parkin mutation

- X-linked dystonia parkinsonism

- Autosomal recessive juvenile parkinsonism

The most recognizable symptoms in Parkinson's disease are movement ("motor") related. Non-motor symptoms, which include autonomic dysfunction, neuropsychiatric problems (mood, cognition, behavior or thought alterations), and sensory (especially altered sense of smell) and sleep difficulties, are also common. Some of these non-motor symptoms may be present at the time of diagnosis.

Four motor symptoms are considered cardinal in PD: tremor, slowness of movement (bradykinesia), rigidity, and postural instability.

The most common presenting sign is a coarse slow tremor of the hand at rest which disappears during voluntary movement of the affected arm and in the deeper stages of sleep. It typically appears in only one hand, eventually affecting both hands as the disease progresses. Frequency of PD tremor is between 4 and 6 hertz (cycles per second). A feature of tremor is "pill-rolling", the tendency of the index finger and thumb to touch and perform together a circular movement. The term derives from the similarity between the movement of people with PD and the early pharmaceutical technique of manually making pills.

Bradykinesia (slowness of movement) is found in every case of PD, and is due to disturbances in motor planning of movement initiation, and associated with difficulties along the whole course of the movement process, from planning to initiation to execution of a movement. Performance of sequential and simultaneous movement is impaired. Bradykinesia is the most handicapping symptom of Parkinson’s disease leading to difficulties with everyday tasks such as dressing, feeding, and bathing. It leads to particular difficulty in carrying out two independent motor activities at the same time and can be made worse by emotional stress or concurrent illnesses. Paradoxically patients with Parkinson's disease can often ride a bicycle or climb stairs more easily than walk on a level. While most physicians may readily notice bradykinesia, formal assessment requires a patient to do repetitive movements with their fingers and feet.

Rigidity is stiffness and resistance to limb movement caused by increased muscle tone, an excessive and continuous contraction of muscles. In parkinsonism the rigidity can be uniform ("lead-pipe rigidity") or ratchety ("cogwheel rigidity"). The combination of tremor and increased tone is considered to be at the origin of cogwheel rigidity. Rigidity may be associated with joint pain; such pain being a frequent initial manifestation of the disease. In early stages of Parkinson's disease, rigidity is often asymmetrical and it tends to affect the neck and shoulder muscles prior to the muscles of the face and extremities. With the progression of the disease, rigidity typically affects the whole body and reduces the ability to move.

Postural instability is typical in the later stages of the disease, leading to impaired balance and frequent falls, and secondarily to bone fractures, loss of confidence, and reduced mobility. Instability is often absent in the initial stages, especially in younger people, especially prior to the development of bilateral symptoms. Up to 40% of people diagnosed with PD may experience falls and around 10% may have falls weekly, with the number of falls being related to the severity of PD.

Other recognized motor signs and symptoms include gait and posture disturbances such as festination (rapid shuffling steps and a forward-flexed posture when walking with no flexed arm swing). Freezing of gait (brief arrests when the feet seem to get stuck to the floor, especially on turning or changing direction), a slurred monotonous quiet voice, mask-like facial expression, and handwriting that gets smaller and smaller are other common signs.

Parkinsonism is a clinical syndrome characterized by tremor, bradykinesia, rigidity, and postural instability. Parkinsonism is found in Parkinson's disease (after which it is named), however a wide range of other causes may lead to this set of symptoms, including some toxins, a few metabolic diseases, and a handful of neurological conditions other than Parkinson's disease.

About 7% of people with parkinsonism have developed their symptoms following treatment with particular medications. Side effect of medications, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and butyrophenones (such as haloperidol), piperazines (such as ziprasidone), and rarely, antidepressants. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level, not progress like Parkinson's disease.

Progressive supranuclear palsy (PSP) is a form of dementia that is characterized by problems with eye movements. Generally the problems begin with difficulty moving the eyes up and/or down (vertical gaze palsy). Since difficulty moving the eyes upward can sometimes happen in normal aging, problems with downward eye movements are the key in PSP. Other key symptoms of PSP include falls backwards, balance problems, slow movements, rigid muscles, irritability, apathy, social withdrawal, and depression. The person may also have certain "frontal lobe signs" such as perseveration, a grasp reflex and utilization behavior (the need to use an object once you see it). People with PSP often have progressive difficulty eating and swallowing, and eventually with talking as well. Because of the rigidity and slow movements, PSP is sometimes misdiagnosed as Parkinson's disease.

On scans of the brain, the midbrain of people with PSP is generally shrunken (atrophied), but there are no other common brain abnormalities visible on images of the person's brain.

Dementia with Lewy bodies (DLB) is a type of dementia that worsens over time. Additional symptoms may include fluctuations in alertness, visual hallucinations, slowness of movement, trouble walking, and rigidity. Excessive movement during sleep and mood changes such as depression are also common.

The cause is unknown. Typically, no family history of the disease exists among those affected. The underlying mechanism involves the buildup of Lewy bodies, clumps of alpha-synuclein protein in neurons. It is classified as a neurodegenerative disorder. A diagnosis may be suspected based on symptoms, with blood tests and medical imaging done to rule out other possible causes. The differential diagnosis includes Parkinson's and Alzheimer's.

At present there is no cure. Treatments are supportive and attempt to relieve some of the motor and psychological symptoms associated with the disease. Acetylcholinesterase inhibitors, such as donepezil, may provide some benefit. Some motor problems may improve with levodopa. Antipsychotics, even for hallucinations, should generally be avoided due to side effects.

DLB is the most common cause of dementia after Alzheimer's disease and vascular dementia. It typically begins after the age of 50. About 0.1% of those over 65 are affected. Men appear to be more commonly affected than women. In the late part of the disease, people may depend entirely on others for their care. Life expectancy following diagnosis is about eight years. The abnormal deposits that cause the disease were discovered in 1912 by Frederic Lewy.

Corticobasal degeneration is a rare form of dementia that is characterized by many different types of neurological problems that get progressively worse over time. This is because the disorder affects the brain in many different places, but at different rates. One common sign is difficulty with using only one limb. One symptom that is extremely rare in any condition other than corticobasal degeneration is the "alien limb." The alien limb is a limb of the person that seems to have a mind of its own, it moves without control of the person's brain. Other common symptoms include jerky movements of one or more limbs (myoclonus), symptoms that are different in different limbs (asymmetric), difficulty with speech that is due to not being able to move the mouth muscles in a coordinated way, numbness and tingling of the limbs and neglecting one side of the person's vision or senses. In neglect, a person ignores the opposite side of the body from the one that has the problem. For example, a person may not feel pain on one side, or may only draw half of a picture when asked. In addition, the person's affected limbs may be rigid or have muscle contractions causing strange repetitive movements (dystonia).

The area of the brain most often affected in corticobasal degeneration is the posterior frontal lobe and parietal lobe. Still, many other part of the brain can be affected.

Parkinson-plus syndromes, also known as disorders of multiple system degeneration, is a group of neurodegenerative diseases featuring the classical features of Parkinson's disease (tremor, rigidity, akinesia/bradykinesia, and postural instability) with additional features that distinguish them from simple idiopathic Parkinson's disease (PD). Some consider Alzheimer's disease to be in this group. Parkinson-plus syndromes are either inherited genetically or occur sporadically.

The atypical parkinsonian or Parkinson-plus syndromes are often difficult to differentiate from PD and each other. They include multiple system atrophy (MSA), progressive supranuclear palsy (PSP), and corticobasal degeneration (CBD). Dementia with Lewy bodies (DLB), may or may not be part of the PD spectrum, but it is increasingly recognized as the second-most common type of neurodegenerative dementia after Alzheimer's disease. These disorders are currently lumped into two groups, the synucleinopathies and the tauopathies. They may coexist with other pathologies.

Additional Parkinson-plus syndromes include Pick's disease and olivopontocerebellar atrophy. The latter is characterized by ataxia and dysarthria, and may occur either as an inherited disorder or as a variant of multiple system atrophy. MSA is also characterized by autonomic failure, formerly known as Shy–Drager syndrome.

Clinical features that distinguish Parkinson-plus syndromes from idiopathic PD include symmetrical onset, a lack of or irregular resting tremor, and a reduced response to dopaminergic drugs (including levodopa). Additional features include bradykinesia, early-onset postural instability, increased rigidity in axial muscles, dysautonomia, alien limb syndrome, supranuclear gaze palsy, apraxia, involvement of the cerebellum including the pyramidal cells, and in some instances significant cognitive impairment.

The initial symptoms in two-thirds of cases are loss of balance, lunging forward when mobilizing, fast walking, bumping into objects or people, and falls.

Other common early symptoms are changes in personality, general slowing of movement, and visual symptoms.

Later symptoms and signs are dementia (typically including loss of inhibition and ability to organize information), slurring of speech, difficulty swallowing, and difficulty moving the eyes, particularly in the vertical direction. The latter accounts for some of the falls experienced by these patients as they are unable to look up or down.

Some of the other signs are poor eyelid function, contracture of the facial muscles, a backward tilt of the head with stiffening of the , sleep disruption, urinary incontinence and constipation.

The visual symptoms are of particular importance in the diagnosis of this disorder. Patients typically complain of difficulty reading due to the inability to look down well. Notably, the ophthalmoparesis experienced by these patients mainly concerns voluntary eye movement and the inability to make vertical saccades, which is often worse with downward saccades. Patients tend to have difficulty looking down (a downgaze ) followed by the addition of an upgaze palsy. This vertical gaze paresis will correct when the examiner passively rolls the patient's head up and down as part of a test for the oculocephalic reflex. Involuntary eye movement, as elicited by Bell's phenomenon, for instance, may be closer to normal. On close inspection, eye movements called "square-wave jerks" may be visible when the patient fixes at distance. These are fine movements, that can be mistaken for nystagmus, except that they are saccadic in nature, with no smooth phase. Difficulties with convergence (convergence insufficiency), where the eyes come closer together while focusing on something near, like the pages of a book, is typical. Because the eyes have trouble coming together to focus at short distances, the patient may complain of diplopia (double vision) when reading.

Cardinal manifestations:

- Supranuclear ophthalmoplegia

- Neck dystonia

- Parkinsonism

- Pseudobulbar palsy

- Behavioral and cognitive impairment

- Imbalance and walking difficulty

- Frequent falls

Accurate diagnosis of these Parkinson-plus syndromes is improved when precise diagnostic criteria are used. Since diagnosis of individual Parkinson-plus syndromes is difficult, the prognosis is often poor. Proper diagnosis of these neurodegenerative disorders is important as individual treatments vary depending on the condition. The nuclear medicine SPECT procedure using I-IBZM, is an effective tool in the establishment of the differential diagnosis between patients with PD and Parkinson-plus syndromes.

Tauopathy belongs to a class of neurodegenerative diseases associated with the pathological aggregation of tau protein in neurofibrillary or gliofibrillary tangles in the human brain. Tangles are formed by hyperphosphorylation of a microtubule-associated protein known as tau, causing it to aggregate in an insoluble form. (These aggregations of hyperphosphorylated tau protein are also referred to as paired helical filaments). The precise mechanism of tangle formation is not completely understood, and it is still controversial as to whether tangles are a primary causative factor in the disease or play a more peripheral role. Primary tauopathies, i.e., conditions in which neurofibrillary tangles (NFT) are predominantly observed, include:

- Primary age-related tauopathy (PART)/Neurofibrillary tangle-predominant senile dementia, with NFTs similar to AD, but without plaques.

- Chronic traumatic encephalopathy, including dementia pugilistica

- Progressive supranuclear palsy

- Corticobasal degeneration

- Frontotemporal dementia and parkinsonism linked to chromosome 17

- Lytico-Bodig disease (Parkinson-dementia complex of Guam)

- Ganglioglioma and gangliocytoma

- Meningioangiomatosis

- Postencephalitic parkinsonism

- Subacute sclerosing panencephalitis

- As well as lead encephalopathy, tuberous sclerosis, Hallervorden-Spatz disease, and lipofuscinosis

Neurofibrillary tangles were first described by Alois Alzheimer in one of his patients suffering from Alzheimer's disease (AD), which is considered a secondary tauopathy. AD is also classified as an amyloidosis because of the presence of senile plaques.

The degree of NFT involvement in AD is defined by Braak stages. Braak stages I and II are used when NFT involvement is confined mainly to the transentorhinal region of the brain, stages III and IV when there's also involvement of limbic regions such as the hippocampus, and V and VI when there's extensive neocortical involvement. This should not be confused with the degree of senile plaque involvement, which progresses differently.

In both Pick's disease and corticobasal degeneration, tau proteins are deposited as inclusion bodies within swollen or "ballooned" neurons.

Argyrophilic grain disease (AGD), another type of dementia, is marked by an abundance of argyrophilic grains and coiled bodies upon microscopic examination of brain tissue. Some consider it to be a type of Alzheimer's disease. It may co-exist with other tauopathies such as progressive supranuclear palsy and corticobasal degeneration, and also Pick's disease.

Huntington's disease (HD): a neurodegenerative disease caused by a CAG tripled expansion in the Huntington gene is the most recently described tauopathy (Fernandez-Nogales et al. Nat Med 2014). JJ Lucas and co-workers demonstrate that, in brains with HD, tau levels are increased and the 4R/3R balance is altered. In addition, the Lucas study shows intranuclear insoluble deposits of tau; these "Lucas' rods" were also found in brains with Alzheimer's disease.

Tauopathies are often overlapped with synucleinopathies, possibly due to interaction between the synuclein and tau proteins.

The non-Alzheimer's tauopathies are sometimes grouped together as "Pick's complex" due to their association with frontotemporal dementia, or frontotemporal lobar degeneration.

PSP is frequently misdiagnosed as Parkinson's disease because of the slowed movements and gait difficulty, or as Alzheimer's disease because of the behavioral changes. It is one of a number of diseases collectively referred to as Parkinson plus syndromes. A poor response to levodopa along with symmetrical onset can help differentiate this disease from PD. Also, patients with the Richardson variant tend to have an upright or arched-back posture as opposed to the stooped-forward posture of other Parkinsonian disorders, although PSP-Parkinsonism (see below) may show the stooped posture. Early falls are characteristic, especially with Richardson-syndrome.

As with bodig, the symptoms and forms of lytico present themselves differently from patient to patient.

Patient presentations include muscle atrophy, maxillofacial paralysis, inability to speak or swallow and subsequent choking. Some patients retain mental lucidity throughout the illness until death, much like ALS patients.

Diaphragm and respiratory accessory muscles can become paralyzed necessitating mechanical ventilation to facilitate breathing. Saliva must be suctioned from the mouth to prevent aspiration. This form of lytico-bodig is fatal in all cases.

No standard form of Bodig has been reported and the documented cases of the disease manifested in many different clinical presentations.

The doctor visited a patient who had just suddenly come down with a virulent form. His symptoms had begun 18 months before, starting with a strange immobility and a loss of initiative and spontaneity; he found he had to make a huge effort to walk, to stand, and to make the least movement—his body was disobedient. The immobility attacked with frightening speed, and within a year, he was unable to stand alone and could not control his posture (2006).

—Oliver Sacks, "The Island of the Colorblind", Vintage Books, 1996

Progressive dementia is also characteristic of bodig. Those who experience dementia are often aphasic and restless, and demonstrate irrational behavior, such as violence, and deep emotions at odd intervals. Patients experience manic highs and lows, giggling one minute and screaming the next.

Patients in the most virulent stage present with mouths hanging open, excessive salivation; their tongues hang motionless, rendering speech and swallowing impossible. The patient’s arms and legs become severely spastic and bent in immovable tension.

The advanced progression presents as profound motionlessness, catatonia, accompanied with tremors or rigidity. Except in cases with concurrent dementia, most patients are capable of lucid thought and speech throughout the disease’s physical progression.

The course of encephalitis lethargica can vary significantly between individuals, particularly when accompanied by preexisting or simultaneous diseases and disorders. It is characterized by high fever, sore throat, headache, lethargy, double vision, delayed physical and mental response, sleep inversion and catatonia. In severe cases, patients may enter a coma-like state (akinetic mutism). Patients may also experience abnormal eye movements ("oculogyric crises"), parkinsonism, upper body weakness, muscular pains, tremors, neck rigidity, and behavioral changes including psychosis. Klazomania (a vocal tic) is sometimes present.

Parkinsonian gait (or festinating gait, from Latin "festinare" [to hurry]) is the type of gait exhibited by patients suffering from Parkinson's disease (PD). This disorder is caused by a deficiency of dopamine in the basal ganglia circuit leading to motor deficits. Gait is one of the most affected motor characteristics of this disorder although symptoms of Parkinson's disease are varied.

Parkinsonian gait is characterized by small shuffling steps and a general slowness of movement (hypokinesia), or even the total loss of movement (akinesia) in the extreme cases. Patients with PD demonstrate reduced stride length and walking speed during free ambulation while double support duration and cadence rate are increased. The patient has difficulty starting, but also has difficulty stopping after starting. This is due to muscle hypertonicity.

Patients with Parkinson's disease exhibit gait characteristics that are markedly different from normal gait. While the list of abnormal gait characteristics given below is the most discussed, it is certainly not exhaustive.

The symptoms have been known to include apathy, dementia, Parkinsonism, agitation, urinary incontinence, and pseudobulbar palsy, among many other neuropsychiatric symptoms.

Microscopically, extensive hemispheric demyelination and the degeneration of basal ganglia are observed.

Encephalitis lethargica or Nellysa disease is an atypical form of encephalitis. Also known as "sleeping sickness" or "sleepy sickness" (distinct from tsetse fly-transmitted sleeping sickness), it was first described in 1917 by the neurologist Constantin von Economo and the pathologist Jean-René Cruchet.

The disease attacks the brain, leaving some victims in a statue-like condition, speechless and motionless. Between 1915 and 1926, an epidemic of encephalitis lethargica spread around the world. Nearly five million people were affected, a third of whom died in the acute stages. Many of those who survived never returned to their pre-existing "aliveness".They would be conscious and aware – yet not fully awake; they would sit motionless and speechless all day in their chairs, totally lacking energy, impetus, initiative, motive, appetite, affect or desire; they registered what went on about them without active attention, and with profound indifference. They neither conveyed nor felt the feeling of life; they were as insubstantial as ghosts, and as passive as zombies.No recurrence of the epidemic has since been reported, though isolated cases continue to occur.

The onset of the symptoms usually occurs several weeks after the initial hypoxic episode. The hypoxic episode is necessarily severe, usually with an arterial oxygen partial pressure less than 40mmHg. Following the severe hypoxia, the patient typically falls unconscious or into a coma, with the exception of cases of carbon monoxide poisoning. If the patient recovers from this unconscious state, usually within 24 hours, it is typically followed by a successful recovery over a few days (generally 4 to 5). After the short recovery, a lucid period is observed, lasting anywhere from 1 to 4 weeks, in which the patient exhibits no symptoms related to the anoxic episode. It is after this period that the degenerative symptoms begin to appear and rapidly grow in severity.

Choreoathetosis is the occurrence of involuntary movements in a combination of chorea (irregular migrating contractions) and athetosis (twisting and writhing).

It is caused by many different diseases and agents. It is a symptom of several diseases, including Lesch-Nyhan Syndrome, phenylketonuria, and Huntington disease.

Choreoathetosis is also a common presentation of dyskinesia as a side effect of levodopa-carbidopa in the treatment of Parkinson disease.

Initial symptoms include restlessness, agitation, malaise, or a fixed stare. Then comes the more characteristically described extreme and sustained upward deviation of the eyes. In addition, the eyes may converge, deviate upward and laterally, or deviate downward. The most frequently reported associated findings are backwards and lateral flexion of the neck, widely opened mouth, tongue protrusion, and ocular pain. However it may also be associated with intensely painful jaw spasm which may result in the breaking of a tooth. A wave of exhaustion may follow an episode. The abrupt termination of the psychiatric symptoms at the conclusion of the crisis is most striking.

Other features that are noted during attacks include mutism, palilalia, eye blinking, lacrimation, pupil dilation, drooling, respiratory dyskinesia, increased blood pressure and heart rate, facial flushing, headache, vertigo, anxiety, agitation, compulsive thinking, paranoia, depression, recurrent fixed ideas, depersonalization, violence, and obscene language.

It is often not realized that in addition to the acute presentation, oculogyric crisis can develop as a recurrent syndrome, triggered by stress, and exposure to the above drugs.