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.

FTD is traditionally difficult to diagnose due to the heterogeneity of the associated symptoms. Signs and symptoms are classified into three groups based on the functions of the frontal and temporal lobes:

- Behavioural variant frontotemporal dementia (BvFTD) is characterized by changes in social behavior and conduct, with loss of social awareness and poor impulse control.

- Semantic dementia (SD) is characterized by the loss of semantic understanding, resulting in impaired word comprehension, although speech remains fluent and grammatically faultless.

- Progressive nonfluent aphasia (PNFA) is characterized by progressive difficulties in speech production.

However, the following abilities in the person with FTD are preserved:

- Perception

- Spatial Skills

- Memory

- Praxis

In later stages of FTD, the clinical phenotypes may overlap. FTD patients tend to struggle with binge eating and compulsive behaviors. These binge eating habits are often associated with abnormal eating behavior including overeating, stuffing oneself with food, changes in food preferences (cravings for more sweets, carbohydrates), eating inedible objects and snatching food from others. Recent findings from structural MRI research have indicated that eating changes in FTD are associated with atrophy (wasting) in the right ventral insula, striatum, and orbitofrontal cortex.

Patients with FTD show marked deficiencies in executive functioning and working memory. Most FTD patients become unable to perform skills that require complex planning or sequencing. In addition to the characteristic cognitive dysfunction, a number of primitive reflexes known as frontal release signs are often able to be elicited. Usually the first of these frontal release signs to appear is the palmomental reflex which appears relatively early in the disease course whereas the palmar grasp reflex and rooting reflex appear late in the disease course.

In rare cases, FTD can occur in patients with motor neuron disease (MND) (typically amyotrophic lateral sclerosis). The prognosis for people with MND is worse when combined with FTD, shortening survival by about a year.

Frontotemporal dementia (FTD) is the clinical presentation of frontotemporal lobar degeneration, which is characterized by progressive neuronal loss predominantly involving the frontal or temporal lobes, and typical loss of over 70% of spindle neurons, while other neuron types remain intact.

It was first described by Arnold Pick in 1892 and was originally called "Pick's disease", a term now reserved for Pick disease, one specific type of frontotemporal dementia. Second only to Alzheimer's disease (AD) in prevalence, FTD accounts for 20% of young-onset dementia cases. Signs and symptoms typically manifest in late adulthood, more commonly between the ages of 55 and 65, approximately equally affecting men and women.

Common signs and symptoms include significant changes in social and personal behavior, apathy, blunting of emotions, and deficits in both expressive and receptive language. Currently, there is no cure for FTD, but there are treatments that help alleviate symptoms.

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

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.

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

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.

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.

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.

There are 3 main histological subtypes found at post-mortem:

- FTLD-tau is characterised by tau positive inclusions often referred to as Pick-bodies. Examples of FTLD-tau include; Pick's disease, corticobasal degeneration, progressive supranuclear palsy.

- FTLD-TDP (or FTLD-U ) is characterised by ubiquitin and TDP-43 positive, tau negative, FUS negative inclusions. The pathological histology of this subtype is so diverse it is subdivided into four subtypes based on the detailed histological findings:

Two physicians independently categorized the various forms of TDP-43 associated disorders. Both classifications were considered equally valid by the medical community, but the physicians in question have jointly proposed a compromise classification to avoid confusion.

- FTLD-FUS; which is characterised by FUS positive cytoplasmic inclusions, intra nuclear inclusions, and neuritic threads. All of which are present in the cortex, medulla, hippocampus, and motor cells of the spinal cord and XIIth cranial nerve.

Dementia lacking distinctive histology (DLDH) is a rare and controversial entity. New analyses have allowed many cases previously described as DLDH to be reclassified into one of the positively defined subgroups.

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.

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.

Frontotemporal lobar degeneration (FTLD) is a pathological process that occurs in frontotemporal dementia. It is characterized by atrophy in the frontal lobe and temporal lobe of the brain, with sparing of the parietal and occipital lobes.

Common proteinopathies that are found in FTLD include the accumulation of Tau proteins and TARDBPs. Mutations in the C9orf72 gene have been established as a major genetic contribution of FTLD, although defects in the GRN and MAPT genes are also associated with it.

Many neuropsychiatric symptoms have been identified in clinical studies of HDLS patients. These include severe depression and anxiety that have been identified in about 70% of HDLS families, verging on suicidal tendencies and substance abuse such as alcoholism. Additionally, patients may exhibit disorientation, confusion, agitation, irritability, aggressiveness, an altered mental state, the loss of the ability to execute learned movements (apraxia), or the inability to speak (mutism).

With symptoms of personality changes, behavioral changes, dementia, depression, and epilepsy, HDLS has been commonly misdiagnosed for a number of other diseases. Dementia or frontotemporal behavioral changes, for example, have commonly steered some clinicians to mistakenly consider diagnoses such as Alzheimer’s disease, frontotemporal dementia or atypical Parkinsonism. The presence of white matter changes has led to misdiagnosis of multiple sclerosis. HDLS commonly manifests with neuropsychiatric symptoms, progressing to dementia, and after a few years shows motor dysfunction. Eventually patients become wheelchair-bound or bedridden.

White matter degeneration is associated with and makes differential diagnoses out of other adult onset leukodystrophies such as metachromatic leukodystrophy (MLD), Krabbe disease (globoid cell leukodystrophy), and X-linked adrenoleukodystrophy (X-ADL).

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.

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.

Ideomotor apraxia (IMA) impinges on one's ability to carry out common, familiar actions on command, such as waving goodbye. Persons with IMA exhibit a loss of ability to carry out motor movements, and may show errors in how they hold and move the tool in attempting the correct function.

One of the defining symptoms of ideomotor apraxia is the inability to pantomime tool use. As an example, if a normal individual were handed a comb and instructed to pretend to brush his hair, he would grasp the comb properly and pass it through his hair. If this were repeated in a patient with ideomotor apraxia, the patient may move the comb in big circles around his head, hold it upside-down, or perhaps try and brush his teeth with it. The error may also be temporal in nature, such as brushing exceedingly slowly. The other characteristic symptom of ideomotor apraxia is the inability to imitate hand gestures, meaningless or meaningful, on request; a meaningless hand gesture is something like having someone make a ninety-degree angle with his thumb and placing it under his nose, with his hand in the plane of his face. This gesture has no meaning attached to it. In contrast, a meaningful gesture is something like saluting or waving goodbye. An important distinction here is that all of the above refer to actions that are consciously and voluntarily initiated. That is to say that a person is specifically asked to either imitate what someone else is doing or is given verbal instructions, such as "wave goodbye." People suffering from ideomotor apraxia will know what they are supposed to do, e.g. they will know to wave goodbye and what their arm and hand should do to accomplish it, but will be unable to execute the motion correctly. This voluntary type of action is distinct from spontaneous actions. Ideomotor apraxia patients may still retain the ability to perform spontaneous motions; if someone they know leaves the room, for instance, they may be able to wave goodbye to that person, despite being unable to do so at request. The ability to perform this sort of spontaneous action is not always retained, however; some sufferers lose this capability, as well. The recognition of meaningful gestures, e.g. understanding what waving goodbye means when it is seen, seems to be unaffected by ideomotor apraxia. It has also been shown that ideomotor apraxia sufferers may have some deficits in general spontaneous movements. Apraxia patients appear to be unable to tap their fingers as quickly as a control group, with a lower maximum tapping rate correlated with more severe apraxia. It has also been demonstrated that apraxic patients are slower to point at a target light when they do not have sight of their hand as compared with healthy patients under the same conditions. The two groups did not differ when they could see their hands. The speed and accuracy of grasping objects also appears unaffected by ideomotor apraxia. Patients suffering from ideomotor apraxia appear to be much more reliant on visual input when conducting movements then nonapraxic individuals.

Acute dystonia nearly always develops a few weeks after a dopamine blocking agent/medication has begun or a substantial increase in antipsychotic dosage. An acute dystonic reaction consists of sustained, painful muscular spasms, producing twisting of the trunk/body and abnormal posture. The most frequent occurrences of these spasms have been reported in the neck, tongue, and jaw. Oculogyric crisis and opisthotonus are also very common. Acute effects of dopamine antagonists also include Parkinsons-like symptoms, manifested by bradykinesia, pin rolling tremor, and rigidity of the body. These movements may fluctuate over hours and temporarily dissipate in response to reassurance, and the individual episodes may last minutes to hours. Acute reactions are more common in older patients and females. The pathophysiology underlying these reactions is unknown, but the movements usually occur during the period when blood medication level is dropping. The acute syndromes which occur due to prolonged exposure to a dopamine antagonist are collectively termed extrapyramidal symptoms, EPS.

Ideomotor Apraxia, often IMA, is a neurological disorder characterized by the inability to correctly imitate hand gestures and voluntarily mime tool use, e.g. pretend to brush one's hair. The ability to spontaneously use tools, such as brushing one's hair in the morning without being instructed to do so, may remain intact, but is often lost. The general concept of apraxia and the classification of ideomotor apraxia were developed in Germany in the late 19th and early 20th centuries by the work of Hugo Liepmann, Adolph Kussmaul, Arnold Pick, Paul Flechsig, Hermann Munk, Carl Nothnagel, Theodor Meynert, and linguist Heymann Steinthal, among others. Ideomotor apraxia was classified as "ideo-kinetic apraxia" by Liepmann due to the apparent dissociation of the idea of the action with its execution. The classifications of the various subtypes are not well defined at present, however, owing to issues of diagnosis and pathophysiology. Ideomotor apraxia is hypothesized to result from a disruption of the system that relates stored tool use and gesture information with the state of the body to produce the proper motor output. This system is thought to be related to the areas of the brain most often seen to be damaged when ideomotor apraxia is present: the left parietal lobe and the premotor cortex. Little can be done at present to reverse the motor deficit seen in ideomotor apraxia, although the extent of dysfunction it induces is not entirely clear.

There are several types of apraxia including:

- Ideomotor apraxia: These patients have deficits in their ability to plan or complete motor actions that rely on semantic memory. They are able to explain how to perform an action, but unable to "imagine" or act out a movement such as "pretend to brush your teeth" or "pucker as though you bit into a sour lemon." However, when the ability to perform an action automatically when cued remains intact, this is known as automatic-voluntary dissociation. For example, they may not be able to pick up a phone when asked to do so, but can perform the action without thinking when the phone rings.

- Ideational/conceptual apraxia: Patients have an inability to conceptualize a task and impaired ability to complete multistep actions. Consists of an inability to select and carry out an appropriate motor program. For example, the patient may complete actions in incorrect orders, such as buttering bread before putting it in the toaster, or putting on shoes before putting on socks. There is also a loss of ability to voluntarily perform a learned task when given the necessary objects or tools. For instance, if given a screwdriver, the patient may try to write with it as if it were a pen, or try to comb his hair with a toothbrush.

- Buccofacial or orofacial apraxia: Non-verbal oral or buccofacial ideomotor apraxia describes difficulty carrying out movements of the face on demand. For example, an inability to lick one's lips or whistle when requested suggests an inability to carry out volitional movements of the tongue, cheeks, lips, pharynx, or larynx on command.

- Constructional apraxia: The inability to draw or construct simple configurations, such as intersecting shapes.

- Gait apraxia: The loss of ability to have normal function of the lower limbs such as walking. This is not due to loss of motor or sensory functions.

- Limb-kinetic apraxia: voluntary movements of extremities are impaired. For example, a person affected by limb apraxia may have difficulty waving hello.

- Oculomotor apraxia: Difficulty moving the eye, especially with saccade movements that direct the gaze to targets. This is one of the 3 major components of Balint's syndrome.

- Apraxia of speech (AOS): Difficulty planning and coordinating the movements necessary for speech (e.g. Potato=Totapo, Topato.) AOS can independently occur without issues in areas such as verbal comprehension, reading comprehension, writing, articulation or prosody.

The predominant symptom of Pisa syndrome is dystonia. Dystonia is a neurological movement disorder characterized by sustained muscle contraction leading to abnormal posture, twisting, and repetitive movement. In Pisa Syndrome specifically there is commonly a tonic flexion of the trunk of the body to one side, leading to a slight lean (reminiscent of the Leaning Tower of Pisa, hence the name "Pisa syndrome"). This is usually associated with a backward axial rotation of the spine and indifferent to markedly abnormal posture. Patients diagnosed with Pisa Syndrome usually experience either acute dystonia or tardive dystonia, also known as tardive dyskinesia. Differential diagnosis between the two may be hard to accomplish without a complete patient history, since both types of dystonia may occur simultaneously in a patient. These symptoms generally disappear after discontinuation of the antipsychotic drug. The time of onset of symptoms may vary depending on drug being administered and the neurological characteristics of the patient in question.

Bálint's syndrome symptoms can be quite debilitating since they impact visuospatial skills, visual scanning and attentional mechanisms. Since it represents impairment of both visual and language functions, it is a significant disability that can affect the patient's safety—even in one's own home environment, and can render the person incapable of maintaining employment. In many cases the complete trio of symptoms—inability to perceive the visual field as a whole (simultanagnosia), difficulty in fixating the eyes (oculomotor apraxia), and inability to move the hand to a specific object by using vision (optic ataxia)—may not be noticed until the patient is in rehabilitation. Therapists unfamiliar with Bálint's syndrome may misdiagnose a patient's inability to meet progress expectations in any of these symptom areas as simply indicating incapability of benefiting from further traditional therapy. The very nature of each Bálint symptom frustrates rehabilitation progress in each of the other symptoms. Much more research is needed to develop therapeutic protocols that address Bálint symptoms as a group since the disabilities are so intertwined.