The main clinical features are signature language progressive difficulties with speech production. There can be problems in different parts of the speech production system, hence patients can present with articulatory breakdown, phonemic breakdown (difficulties with sounds) and other problems. However, it is rare for patients to have just one of these problems and most people will present with more than one problem. Features include:

- Hesitant, effortful speech

- Speech 'apraxia'

- Stutter (including return of a childhood stutter)

- Anomia

- Phonemic paraphasia (sound errors in speech e.g. 'gat' for 'cat')

- Agrammatism (using the wrong tense or word order)

As the disease develops, speech quantity decreases and many patients will become mute.

Cognitive domains other than language are rarely affected early on. However, as the disease progresses other domains can be affected. Problems with writing, reading and speech comprehension can occur as can behavioural features similar to frontotemporal dementia.

Three classifications of primary progressive aphasia have been described. In the classical Mesulam criteria for primary progressive aphasia, there are two variants: a non-fluent type progressive nonfluent aphasia (PNFA) and a fluent type semantic dementia (SD). A third variant of primary progressive aphasia, logopenic progressive aphasia (LPA), is an atypical form of Alzheimer's disease. Early PNFA can include such features as speech apraxia, effortful speech, and anomia, and thus can resemble Broca’s aphasia. Early LPA involves impairments in naming and sentence repetition, and thus can resemble Conduction aphasia. However, these PPA subtypes differ from these similar aphasias, as these subtypes do not occur acutely following trauma to the brain, such as following a stroke, due to differing functional and structural neuroanatomical patterns of involvement and the progressive nature of the disease.

Progressive nonfluent aphasia (PNFA) is one of three clinical syndromes associated with frontotemporal lobar degeneration. PNFA has an insidious onset of language deficits over time as opposed to other stroke-based aphasias, which occur acutely following trauma to the brain. The specific degeneration of the frontal and temporal lobes in PNFA creates hallmark language deficits differentiating this disorder from other Alzheimer-type disorders by the initial absence of other cognitive and memory deficits. This disorder commonly has a primary effect on the left hemisphere, causing the symptomatic display of expressive language deficits (production difficulties) and sometimes may disrupt receptive abilities in comprehending grammatically complex language.

Gerstmann syndrome is characterized by four primary symptoms:

1. Dysgraphia/agraphia: deficiency in the ability to write

2. Dyscalculia/acalculia: difficulty in learning or comprehending mathematics

3. Finger agnosia/anomia: inability to distinguish the fingers on the hand

4. Left-right disorientation

Primary progressive aphasia (PPA) is a type of neurological syndrome in which language capabilities slowly and progressively become impaired. As with other types of aphasia, the symptoms that accompany PPA depend on what parts of the left hemisphere are significantly damaged. However, unlike most other aphasias, PPA results from continuous deterioration in brain tissue, which leads to early symptoms being far less detrimental than later symptoms. Those with PPA slowly lose the ability to speak, write, read, and generally comprehend language. Eventually, almost every patient becomes mute and completely loses the ability to understand both written and spoken language. Although it was first described as solely impairment of language capabilities while other mental functions remain intact, it is now recognized that many, if not most of those afflicted suffer impairment of memory, short term memory formation and loss of executive functions. It was first described as a distinct syndrome by M.-Marsel Mesulam in 1982. Primary progressive aphasias have a clinical and pathological overlap with the frontotemporal lobar degeneration (FTLD) spectrum of disorders and Alzheimer's disease. However, PPA is not considered synonymous to Alzheimer's disease due to the fact that, unlike those affected by Alzheimer's disease, those with PPA are generally able to maintain the ability to care for themselves, remain employed, and pursue interests and hobbies. Moreover, in diseases such as Alzheimer's disease, Pick's disease, and Creutzfeld-Jakob disease, progressive deterioration of comprehension and production of language is just one of the many possible types of mental deterioration, such as the progressive decline of memory, motor skills, reasoning, awareness, and visuospatial skills.

The bilateral form of FCMS ("also known as facio-labio-pharyngo-glosso-laryngo-brachial paralysis)" is consistent with the classic presentation of bilateral corticobulbar involvement. It is characterized by well-preserved automatic and reflex movements. It is caused by lesions in the cortical or subcortical region of the anterior opercular area surrounding the insula forming the gyri of the frontal, temporal, and parietal lobes.

This disorder is often associated with brain lesions in the dominant (usually left) hemisphere including the angular and supramarginal gyri (Brodmann area 39 and 40 respectively) near the temporal and parietal lobe junction. There is significant debate in the scientific literature as to whether Gerstmann Syndrome truly represents a unified, theoretically motivated syndrome. Thus its diagnostic utility has been questioned by neurologists and neuropsychologists alike. The angular gyrus is generally involved in translating visual patterns of letter and words into meaningful information, such as is done while reading.

Dysarthrias are classified in multiple ways based on the presentation of symptoms. Specific dysarthrias include spastic (resulting from bilateral damage to the upper motor neuron), flaccid (resulting from bilateral or unilateral damage to the lower motor neuron), ataxic (resulting from damage to cerebellum), unilateral upper motor neuron (presenting milder symptoms than bilateral UMN damage), hyperkinetic and hypokinetic (resulting from damage to parts of the basal ganglia, such as in Huntington's disease or Parkinsonism), and the mixed dysarthrias (where symptoms of more than one type of dysarthria are present). The majority of dysarthric patients are diagnosed as having 'mixed' dysarthria, as neural damage resulting in dysarthria is rarely contained to one part of the nervous system — for example, multiple strokes, traumatic brain injury, and some kinds of degenerative illnesses (such as amyotrophic lateral sclerosis) usually damage many different sectors of the nervous system.

Ataxic dysarthria is an acquired neurological and sensorimotor speech deficit. It is a common diagnosis among the clinical spectrum of ataxic disorders. Since regulation of skilled movements is a primary function of the cerebellum, damage to the superior cerebellum and the superior cerebellar peduncle is believed to produce this form of dysarthria in ataxic patients. Growing evidence supports the likelihood of cerebellar involvement specifically affecting speech motor programming and execution pathways, producing the characteristic features associated with ataxic dysarthria. This link to speech motor control can explain the abnormalities in articulation and prosody, which are hallmarks of this disorder. Some of the most consistent abnormalities observed in patients with ataxia dysarthria are alterations of the normal timing pattern, with prolongation of certain segments and a tendency to equalize the duration of syllables when speaking. As the severity of the dysarthria increases, the patient may also lengthen more segments as well as increase the degree of lengthening of each individual segment.

Common clinical features of ataxic dysarthria include abnormalities in speech modulation, rate of speech, explosive or scanning speech, slurred speech, irregular stress patterns, and vocalic and consonantal misarticulations.

Ataxic dysarthria is associated with damage to the left cerebellar hemisphere in right-handed patients.

Dysarthria may affect a single system; however, it is more commonly reflected in multiple motor-speech systems. The etiology, degree of neuropathy, existence of co-morbidities, and the individual's response all play a role in the effect the disorder has on the individual's quality of life. Severity ranges from occasional articulation difficulties to verbal speech that is completely unintelligible.

Individuals with dysarthria may experience challenges in the following:

- Timing

- Vocal quality

- Pitch

- Volume

- Breath control

- Speed

- Strength

- Steadiness

- Range

- Tone

Examples of specific observations include a continuous breathy voice, irregular breakdown of articulation, monopitch, distorted vowels, word flow without pauses, and hypernasality.

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

Palilalia is considered an aphasia, a disorder of language, and is not to be confused with speech disorders, as there is no difficulty in the formation of internal speech. Palilalia is similar to speech disorders such as stuttering or cluttering, as it tends to only express itself in spontaneous speech, such as answering basic questions, and not in automatic speech such as reading or singing; however, it distinctively affects words and phrases rather than syllables and sounds.

Palilalia may occur in conditions affecting the pre-frontal cortex or basal ganglia regions, either from physical trauma, neurodegenerative disorders, genetic disorders, or a loss of dopamine in these brain regions. Palilalia occurs most commonly in Tourette syndrome and may be present in neurodegenerative disorders like Alzheimer's disease and progressive supranuclear palsy.

Aphasia in CBD is revealed through the inability to speak or a difficulty in initiating spoken dialogue and falls under the non-fluent (as opposed to fluent or flowing) subtype of the disorder. This may be related to speech impairment such as dysarthria, and thus is not a true aphasia, as aphasia is related to a change in language function, such as difficulty retrieving words or putting words together to form meaningful sentences. The speech and/or language impairments in CBD result in disconnected speech patterns and the omission of words. Individuals with this symptom of CBD often lose the ability to speak as the disease progresses.

Palilalia is defined as the repetition of the speaker's words or phrases, often for a varying number of repeats. Repeated units are generally whole sections of words and are larger than a syllable, with words being repeated the most often, followed by phrases, and then syllables or sounds.

A 2007 case study by Van Borsel "et al." examined the acoustic features in palilalia. AB, a 60-year-old male was diagnosed with idiopathic Parkinson's disease and had noticed changes in gait, posture, writing, and speech. Observation of his perceptual speech characteristics and Frenchay Dysarthria Assessment results suggested AB suffered from hypokinetic dysarthria with a marked palilalia. It was determined to start speech therapy with passive (metronome) and active (pacing boards) pacing techniques to reduce the number of palilalic repetitions. Unfortunately AB was not able to enunciate despite extensive training.

Analysis of AB's speech therapy showed that his repetitions lasted from 1 minute 33 seconds to 2 minutes 28 seconds, ranging from 1 to 32 repetitions on some words, and differed from trial to trial. Pauses were present between each repetition, ranging from 0.1 to 0.7 seconds. Van Borsel "et al." concluded that AB's palilalic repetitions followed no pattern: the duration of each repetition train did not decrease over time, the number of repetitions per train did not increase, and the duration of each individual word did not decrease in duration. Such results indicated not all palilalic repetitions show an increasing rate with decreasing volume, and defied the two distinct subtypes of palilalia as suggested by Sterling. Sterling's Type A, sometimes called "palilalie spasmodique", is characterized by fast repetitions and decreasing volume, while Sterling's Type B, sometimes called "palilalie atonique", is characterized by repetitions at a constant rate with interspersed periods of silence. AB showed neither a systematic increase (Sterling's Type A) or a constant duration (Sterling's Type B) and instead fell between the two.

Palilalia has been theorized to occur in writing and sign language. A case study by Tyrone and Moll examined a 79-year-old right-handed deaf man named PSP who showed anomalies in his signing. PSP had learned British sign language (BSL) at the age of seven and had developed left-sided weakness and dysphagia at age 77. PSP showed involuntary movements and repetitions in his signing. Tyrone and Moll reported his movements were palilalic in nature, as entire signs were repeated and the repetitional movements became smaller and smaller in amplitude.

Ideomotor apraxia (IMA), although clearly present in CBD, often manifests atypically due to the additional presence of bradykinesia and rigidity in those individuals exhibiting the disorders. The IMA symptom in CBD is characterized by the inability to repeat or mimic particular movements (whether significant or random) both with or without the implementation of objects. This form of IMA is present in the hands and arms, while IMA in the lower extremities may cause problems with walking. Those with CBD that exhibit IMA may appear to have trouble initiating walking, as the foot may appear to be fixed to floor. This can cause stumbling and difficulties in maintaining balance. IMA is associated with deterioration in the premotor cortex, parietal association areas, connecting white matter tracts, thalamus, and basal ganglia. Some individuals with CBD exhibit limb-kinetic apraxia, which involves dysfunction of more fine motor movements often performed by the hands and fingers.

The unilateral operculum syndrome is a very rare form of FCMS caused by the formation of unilateral lesions. In this form of FCMS, the unaffected hemisphere of the brain compensates for the unilateral lesion. Usually, this occurs when the unaffected region is the individual's dominant hemisphere.

The main symptom resulting from PCA is a decrease in visuospatial and visuoperceptual capabilities. Because the posterior region of the brain is home to the occipital lobe, which is responsible for visual processing, visual functions are impaired in PCA patients. The atrophy is progressive; early symptoms include difficulty reading, blurred vision, light sensitivity, issues with depth perception, and trouble navigating through space. Additional symptoms include apraxia, a disorder of movement planning, alexia, an impaired ability to read, and visual agnosia, an object recognition disorder. Damage to the ventral, or “what” stream, of the visual system, located in the temporal lobe, leads to the symptoms related to general vision and object recognition deficits; damage to the dorsal, or “where/how” stream, located in the parietal lobe, leads to PCA symptoms related to impaired movements in response to visual stimuli, such as navigation and apraxia.

As neurodegeneration spreads, more severe symptoms emerge, including the inability to recognize familiar people and objects, trouble navigating familiar places, and sometimes visual hallucinations. In addition, patients may experience difficulty making guiding movements towards objects, and may experience a decline in literacy skills including reading, writing, and spelling. Furthermore, if neural death spreads into other anterior cortical regions, symptoms similar to Alzheimer's disease, such as memory loss, may result. PCA patients with significant atrophy in one hemisphere of the brain may experience hemispatial neglect, the inability to see stimuli on one half of the visual field. Anxiety and depression are also common in PCA patients.

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.

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.

Motor speech disorders are a class of speech disorders that disturb the body's natural ability to speak due to neurologic impairments. These neurologic impairments make it difficult for individuals with motor speech disorders to plan, program, control, coordinate, and execute speech productions. Disturbances to the individual's natural ability to speak vary in their etiology based on the integrity and integration of cognitive, neuromuscular, and musculoskeletal activities. Speaking is an act dependent on thought and timed execution of airflow and oral motor / oral placement of the lips, tongue, and jaw that can be disrupted by weakness in oral musculature (dysarthria) or an inability to execute the motor movements needed for specific speech sound production (apraxia of speech or developmental verbal dyspraxia). Such deficits can be related to pathology of the nervous system (central and /or peripheral systems involved in motor planning) that affect the timing of respiration, phonation, prosody, and articulation in isolation or in conjunction.

There are many potential causes of dysarthria. They include toxic, metabolic, degenerative diseases, traumatic brain injury, or thrombotic or embolic stroke.

Degenerative diseases include parkinsonism, amyotrophic lateral sclerosis (ALS), multiple sclerosis, Huntington's disease, Niemann-Pick disease, and Friedreich ataxia.

Toxic and metabolic conditions include: Wilson's disease, hypoxic encephalopathy such as in drowning, and central pontine myelinolysis.

These result in lesions to key areas of the brain involved in planning, executing, or regulating motor operations in skeletal muscles (i.e. muscles of the limbs), including muscles of the head and neck (dysfunction of which characterises dysarthria). These can result in dysfunction, or failure of: the motor or somatosensory cortex of the brain, corticobulbar pathways, the cerebellum, basal nuclei (consisting of the putamen, globus pallidus, caudate nucleus, substantia nigra etc.), brainstem (from which the cranial nerves originate), or the neuro-muscular junction (in diseases such as myasthenia gravis) which block the nervous system's ability to activate motor units and effect correct range and strength of movements.

Causes:

- Brain tumor

- Cerebral palsy

- Guillain–Barré syndrome

- Hypothermia

- Lyme disease

- Stroke

- Intracranial hypertension (formerly known as pseudotumor cerebri)

- Tay-Sachs, and late onset Tay-Sachs (LOTS), disease

Posterior cortical atrophy (PCA), also called Benson's syndrome, is a form of dementia which is usually considered an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.

In rare cases, PCA can be caused by dementia with Lewy bodies and Creutzfeldt–Jakob disease.

PCA usually affects people at an earlier age than typical cases of Alzheimer's disease, with initial symptoms often experienced in people in their mid-fifties or early sixties. This was the case with writer Terry Pratchett (1948-2015), who went public in 2007 about being diagnosed with PCA. In "The Mind's Eye", neurologist Oliver Sacks examines the case of concert pianist Lilian Kallir (1931–2004), who suffered from PCA.

AOS and expressive aphasia (also known as Broca's aphasia) are commonly mistaken as the same disorder mainly because they often occur together in patients. Although both disorders present with symptoms such as a difficulty producing sounds due to damage in the language parts of the brain, they are not the same. The main difference between these disorders lies in the ability to comprehend spoken language; patients with apraxia are able to fully comprehend speech, while patients with aphasia are not always fully able to comprehend others' speech.

Conduction aphasia is another speech disorder that is similar to, but not the same as, apraxia of speech. Although patients who suffer from conduction aphasia have full comprehension of speech, as do AOS sufferers, there are differences between the two disorders. Patients with conduction aphasia are typically able to speak fluently, but they do not have the ability to repeat what they hear.

Similarly, dysarthria, another motor speech disorder, is characterized by difficulty articulating sounds. The difficulty in articulation does not occur due in planning the motor movement, as happens with AOS. Instead, dysarthria is caused by inability in or weakness of the muscles in the mouth, face, and respiratory system.

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.

Dysarthria is the reduced ability to motor plan volitional movements needed for speech production as the result of weakness/paresis and/or paralysis of the musculature of the oral mechanism needed for respiration, phonation, resonance, articulation, and/or prosody.

Developmental verbal dyspraxia (DVD), also known as childhood apraxia of speech (CAS) and developmental apraxia of speech (DAS), is when children have problems saying sounds, syllables, and words. This is not because of muscle weakness or paralysis. The brain has problems planning to move the body parts (e.g., lips, jaw, tongue) needed for speech. The child knows what they want to say, but their brain has difficulty coordinating the muscle movements necessary to say those words. The exact cause of this disorder is unknown. Some observations suggest a genetic cause of DVD, as many with the disorder have a family history of communication disorders. There is no cure for DVD, but with appropriate, intensive intervention, people with this motor speech disorder can improve significantly.

Progressive supranuclear palsy (PSP; or the Steele–Richardson–Olszewski syndrome, after the doctors who described it in 1963) is a degenerative disease involving the gradual deterioration and death of specific volumes of the brain.

Males and females are affected approximately equally and there is no racial, geographical or occupational predilection. Approximately six people per 100,000 population have PSP.

It has been described as a tauopathy.