Uncrossed tracts of motor nerves from the brain to the anterior horns of the spinal cord, involved in reflexes, locomotion, complex movements, and postural control.
Diseases of the BASAL GANGLIA including the PUTAMEN; GLOBUS PALLIDUS; claustrum; AMYGDALA; and CAUDATE NUCLEUS. DYSKINESIAS (most notably involuntary movements and alterations of the rate of movement) represent the primary clinical manifestations of these disorders. Common etiologies include CEREBROVASCULAR DISORDERS; NEURODEGENERATIVE DISEASES; and CRANIOCEREBRAL TRAUMA.
Agents that control agitated psychotic behavior, alleviate acute psychotic states, reduce psychotic symptoms, and exert a quieting effect. They are used in SCHIZOPHRENIA; senile dementia; transient psychosis following surgery; or MYOCARDIAL INFARCTION; etc. These drugs are often referred to as neuroleptics alluding to the tendency to produce neurological side effects, but not all antipsychotics are likely to produce such effects. Many of these drugs may also be effective against nausea, emesis, and pruritus.
A phenyl-piperidinyl-butyrophenone that is used primarily to treat SCHIZOPHRENIA and other PSYCHOSES. It is also used in schizoaffective disorder, DELUSIONAL DISORDERS, ballism, and TOURETTE SYNDROME (a drug of choice) and occasionally as adjunctive therapy in INTELLECTUAL DISABILITY and the chorea of HUNTINGTON DISEASE. It is a potent antiemetic and is used in the treatment of intractable HICCUPS. (From AMA Drug Evaluations Annual, 1994, p279)
A condition characterized by inactivity, decreased responsiveness to stimuli, and a tendency to maintain an immobile posture. The limbs tend to remain in whatever position they are placed (waxy flexibility). Catalepsy may be associated with PSYCHOTIC DISORDERS (e.g., SCHIZOPHRENIA, CATATONIC), nervous system drug toxicity, and other conditions.
A muscarinic antagonist that crosses the blood-brain barrier and is used in the treatment of drug-induced extrapyramidal disorders and in parkinsonism.
A condition associated with the use of certain medications and characterized by an internal sense of motor restlessness often described as an inability to resist the urge to move.
A selective blocker of DOPAMINE D2 RECEPTORS and SEROTONIN 5-HT2 RECEPTORS that acts as an atypical antipsychotic agent. It has been shown to improve both positive and negative symptoms in the treatment of SCHIZOPHRENIA.
A tricylic dibenzodiazepine, classified as an atypical antipsychotic agent. It binds several types of central nervous system receptors, and displays a unique pharmacological profile. Clozapine is a serotonin antagonist, with strong binding to 5-HT 2A/2C receptor subtype. It also displays strong affinity to several dopaminergic receptors, but shows only weak antagonism at the dopamine D2 receptor, a receptor commonly thought to modulate neuroleptic activity. Agranulocytosis is a major adverse effect associated with administration of this agent.
Conditions which feature clinical manifestations resembling primary Parkinson disease that are caused by a known or suspected condition. Examples include parkinsonism caused by vascular injury, drugs, trauma, toxin exposure, neoplasms, infections and degenerative or hereditary conditions. Clinical features may include bradykinesia, rigidity, parkinsonian gait, and masked facies. In general, tremor is less prominent in secondary parkinsonism than in the primary form. (From Joynt, Clinical Neurology, 1998, Ch38, pp39-42)
A group of inherited and sporadic disorders which share progressive ataxia in combination with atrophy of the CEREBELLUM; PONS; and inferior olivary nuclei. Additional clinical features may include MUSCLE RIGIDITY; NYSTAGMUS, PATHOLOGIC; RETINAL DEGENERATION; MUSCLE SPASTICITY; DEMENTIA; URINARY INCONTINENCE; and OPHTHALMOPLEGIA. The familial form has an earlier onset (second decade) and may feature spinal cord atrophy. The sporadic form tends to present in the fifth or sixth decade, and is considered a clinical subtype of MULTIPLE SYSTEM ATROPHY. (From Adams et al., Principles of Neurology, 6th ed, p1085)
Incoordination of voluntary movements that occur as a manifestation of CEREBELLAR DISEASES. Characteristic features include a tendency for limb movements to overshoot or undershoot a target (dysmetria), a tremor that occurs during attempted movements (intention TREMOR), impaired force and rhythm of diadochokinesis (rapidly alternating movements), and GAIT ATAXIA. (From Adams et al., Principles of Neurology, 6th ed, p90)
A heterogenous group of degenerative syndromes marked by progressive cerebellar dysfunction either in isolation or combined with other neurologic manifestations. Sporadic and inherited subtypes occur. Inheritance patterns include autosomal dominant, autosomal recessive, and X-linked.
A sporadic neurodegenerative disease with onset in middle-age characterized clinically by Parkinsonian features (e.g., MUSCLE RIGIDITY; HYPOKINESIA; stooped posture) and HYPOTENSION. This condition is considered a clinical variant of MULTIPLE SYSTEM ATROPHY. Pathologic features include a prominent loss of neurons in the zona compacta of the SUBSTANTIA NIGRA and PUTAMEN. (From Adams et al., Principles of Neurology, 6th ed, p1075-6)
Disorders of speech articulation caused by imperfect coordination of pharynx, larynx, tongue, or face muscles. This may result from CRANIAL NERVE DISEASES; NEUROMUSCULAR DISEASES; CEREBELLAR DISEASES; BASAL GANGLIA DISEASES; BRAIN STEM diseases; or diseases of the corticobulbar tracts (see PYRAMIDAL TRACTS). The cortical language centers are intact in this condition. (From Adams et al., Principles of Neurology, 6th ed, p489)
A syndrome complex composed of three conditions which represent clinical variants of the same disease process: STRIATONIGRAL DEGENERATION; SHY-DRAGER SYNDROME; and the sporadic form of OLIVOPONTOCEREBELLAR ATROPHIES. Clinical features include autonomic, cerebellar, and basal ganglia dysfunction. Pathologic examination reveals atrophy of the basal ganglia, cerebellum, pons, and medulla, with prominent loss of autonomic neurons in the brain stem and spinal cord. (From Adams et al., Principles of Neurology, 6th ed, p1076; Baillieres Clin Neurol 1997 Apr;6(1):187-204; Med Clin North Am 1999 Mar;83(2):381-92)

Effects of stimulants of abuse on extrapyramidal and limbic neuropeptide Y systems. (1/33)

Neuropeptide Y (NPY), an apparent neuromodulating neuropeptide, has been linked to dopamine systems and dopamine-related psychotic disorders. Because of this association, we determined and compared the effects of psychotomimetic drugs on extrapyramidal and limbic NPY systems. We observed that phencyclidine, methamphetamine (METH), (+)methylenedioxymethamphetamine (MDMA), and cocaine, but not (-)MDMA, similarly reduced the striatal content of NPY-like immunoreactivity from 54% (phencyclidine) to 74% [(+) MDMA] of control. The effects of METH on NPY levels in the nucleus accumbens, caudate nucleus, globus pallidus, and substantia nigra were characterized in greater detail. We observed that METH decreased NPY levels in specific regions of the nucleus accumbens and the caudate, but had no effect on NPY in the globus pallidus or the substantia nigra. The dopamine D1 receptor antagonist SCH-23390 blocked these effects of METH, suggesting that NPY levels throughout the nucleus accumbens and the caudate are regulated through D1 pathways. The D2 receptor antagonist eticlopride did not appear to alter the METH effect, but this was difficult to determine because eticlopride decreased NPY levels by itself. A single dose of METH was sufficient to lower NPY levels, in some, but not all, regions examined. The effects on NPY levels after multiple METH administrations were substantially greater and persisted up to 48 h after treatment; this suggests that synthesis of this neuropeptide may be suppressed even after the drug is gone. These findings suggest that NPY systems may contribute to the D1 receptor-mediated effects of the psychostimulants.  (+info)

Extrapyramidal involvement in amyotrophic lateral sclerosis: backward falls and retropulsion. (2/33)

Three patients with sporadic amyotrophic lateral sclerosis (ALS) presented with a history of backward falls. Impaired postural reflexes and retropulsion accompanied clinical features of ALS. Hypokinesia, decreased arm swing, and a positive glabellar tap were noted in two of these three patients. Cognitive impairment, tremor, axial rigidity, sphincter dysfunction, nuchal dystonia, dysautonomia, and oculomotor dysfunction were absent. Brain MRI disclosed bilateral T2 weighted hyperintensities in the internal capsule and globus pallidus in one patient. Necropsy studies performed late in the course of ALS have shown degeneration in extrapyramidal sites-for example, the globus pallidus, thalamus, and substantia nigra. Clinically, backward falls and retropulsion may occur early in ALS. This may reflect extrapyramidal involvement.  (+info)

S18327 (1-[2-[4-(6-fluoro-1, 2-benzisoxazol-3-yl)piperid-1-yl]ethyl]3-phenyl imidazolin-2-one), a novel, potential antipsychotic displaying marked antagonist properties at alpha(1)- and alpha(2)-adrenergic receptors: II. Functional profile and a multiparametric comparison with haloperidol, clozapine, and 11 other antipsychotic agents. (3/33)

S18327 was dose-dependently active in several models of potential antipsychotic activity involving dopaminergic hyperactivity: inhibition of apomorphine-induced climbing in mice, of cocaine- and amphetamine-induced hyperlocomotion in rats, and of conditioned avoidance responses in rats. Furthermore, reflecting its high affinity at serotonin(2A) sites, S18327 potently blocked phencyclidine-induced locomotion and 1-[2, 5-dimethoxy-4-iodophenyl]-2-aminopropane-induced head-twitches in rats. In models of glutamatergic hypoactivity, S18327 blocked hyperlocomotion and spontaneous tail-flicks elicited by the N-methyl-D-aspartate antagonist dizocilpine. The actions of S18327, together with its binding profile at multiple monoaminergic receptors (15 parameters in total), were compared with those of clozapine, haloperidol, and 11 other antipsychotics by multiparametric analysis, and the resulting dendrogram positioned S18327 close to clozapine. Consistent with a clopazine-like profile, S18327 generalized to a clozapine discriminative stimulus and evoked latent inhibition in rats, blocked aggression in isolated mice, and displayed anxiolytic properties in the ultrasonic vocalization and Vogel procedures in rats. Relative to the above paradigms, only markedly (>20-fold) higher doses of S18327 were active in models predictive of potential extrapyramidal side effects: induction of catalepsy and prolactin secretion, and inhibition of methylphenidate-induced gnawing in rats. S18327 showed only modest affinity for histaminic and muscarinic receptors. Multiparametric analysis of these data distinguished S18327 from both haloperidol (high extrapyramidal potential) and clozapine (high histaminic and muscarinic affinity). In conclusion, S18327 displays a broad-based pattern of potential antipsychotic activity at doses appreciably lower than those eliciting extrapyramidal side effects. In this respect, S18327 closely resembles clozapine, but it is chemically distinct and displays weak affinity for histaminic and muscarinic receptors.  (+info)

Organization of nonprimary motor cortical inputs on pyramidal and nonpyramidal tract neurons of primary motor cortex: An electrophysiological study in the macaque monkey. (4/33)

To elucidate the functions of nonprimary motor cortical (nPMC) areas whose afferents synapse onto output neurons of the primary motor cortex (PMC), we examined the responses of pyramidal tract neurons (PTNs) and non-PTNs (nPTNs) to electrical stimulation in the three nPMCs, the supplementary motor area (SMA) and the dorsal and ventral divisions of the premotor cortex (PMd and PMv), with extracellular unit recording in alert monkeys. Typical responses of PTNs to nPMC stimulation were early orthodromic excitatory responses followed by inhibitory responses. Among 27 PTNs tested by constructing peri-stimulus time histograms, 19 (70.4%) showed inhibitory responses to stimulation in all of the nPMC areas. In contrast, 5/33 PTNs (15.2%) and 10/72 nPTNs (13.9%) showed excitatory responses to stimulation in all of the nPMCs. The inhibitory responses of PTNs were mediated by inhibitory interneurons, some of which may correspond to nPTNs in the superficial layers of the PMC. These interneurons probably possess widely extended axons and nonspecifically inhibit multiple PTNs in layer V. The excitatory and inhibitory influences, and the patterns of convergence of inputs from the nPMCs onto the PTNs, are important to understand motor control by the nPMC-PMC-spinal cord pathway.  (+info)

S33084, a novel, potent, selective, and competitive antagonist at dopamine D(3)-receptors: II. Functional and behavioral profile compared with GR218,231 and L741,626. (5/33)

The selective dopamine D(3)-receptor antagonist S33084 dose dependently attenuated induction of hypothermia by 7-hydroxy-2-dipropylaminotetralin (7-OH-DPAT) and PD128,907. S33084 also dose dependently reduced 7-OH-DPAT-induced penile erections (PEs) but had little effect on 7-OH-DPAT-induced yawning and hypophagia, and it did not block contralateral rotation elicited by the preferential D(3) agonist quinpirole in unilateral substantia nigra-lesioned rats. In models of potential antipsychotic activity, S33084 had little effect on conditioned avoidance behavior and the locomotor response to amphetamine and cocaine in rats, and weakly inhibited apomorphine-induced climbing in mice. Moreover, S33084 was inactive in models of potential extrapyramidal activity in rats: induction of catalepsy and prolactin secretion and inhibition of methylphenidate-induced gnawing. Another selective D(3) antagonist, GR218,231, mimicked S33084 in inhibiting 7-OH-DPAT-induced PEs and hypothermia but neither hypophagia nor yawning behavior. Similarly, it was inactive in models of potential antipsychotic and extrapyramidal activity. In distinction to S33084 and GR218,231, the preferential D(2) antagonist L741,626 inhibited all responses elicited by 7-OH-DPAT. Furthermore, it displayed robust activity in models of antipsychotic and, at slightly higher doses, extrapyramidal activity. In summary, S33084 was inactive in models of potential antipsychotic and extrapyramidal activity and failed to modify spontaneous locomotor behavior. Furthermore, it did not affect hypophagia or yawns, but attenuated hypothermia and PEs, elicited by 7-OH-DPAT. This profile was shared by GR218,231, whereas L741,626 was effective in all models. Thus, D(2)-receptors are principally involved in these paradigms, although D(3)-receptors may contribute to induction of hypothermia and PEs. S33084 should comprise a useful tool for further exploration of the pathophysiological significance of D(3)- versus D(2)-receptors.  (+info)

Extrapyramidal effects of neuroleptics. (6/33)

A study was conducted on 66 psychiatric inpatients who took major tranquilizers for periods of four to 16 years. The frequency of signs of Parkinsonism and the effects of orphenadrine on these were studied in a double-blind crossover method. Sixty-one per cent of the patients showed signs of Parkinsonism. Female patients and those with organic brain pathology more frequently exhibited Parkinsonism (although the difference was not statistically significant). No correlation was found between duration of treatment and extrapyramidal effects. Of the 40 patients who developed Parkinsonism, 25 responded favourably to orphenadrine, while six (15%) had more marked manifestations on orphenadrine than on placebo.  (+info)

Cortical and long spinal actions on lumbosacral motoneurones in the cat. (7/33)

1. The effects of stimulating forelimb afferents on various ipsilateral motoneurones of the hind limb have been compared with those of volleys set up in the contralateral pericruciate cortex in cats anaesthetized with chloralose. 2. With intact neuraxis, brachial plexus volleys evoke discharge of flexor and extensor motoneurones; short cortical tetani also elicit discharge mainly of flexor motoneurons. After a pyramid-sparing brainstem lesion, little or no firing is evoked by either input. 3. Monosynaptic reflex testing and intracellular recording reveal subthreshold actions on hind-limb motoneurones, inhibition of FDHL and later facilitation of extensors and flexors by forelimb volleys, facilitation of flexors and extensors together with inconstant inhibition of the latter, by cortical stimulation. 4. Interruption of medullary extrapyramidal paths greatly reduces intensity and duration of facilitation from the forelimb, and largely removes cortically evoked extensor facilitation. Inhibition of FDHL from forelimb and cortex is unchanged; cortical volleys continue to facilitate flexors, and have mainly inhibitory action on extensors in these 'pyramidal' preparations. 5. Hyperpolarization of FDHL motoneurones occurs in response to forelimb and cortical volleys, of time course corresponding to depression of test reflexes. Spinal pathways responsible for the two inhibitory actions are independent, and unless each is very strong, their separate actions summate when elicited together. 6. Receptive field for FDHL inhibition from the forelimb is located distally in the forepaw, and its receptors are largely served by cutaneous fibres of low threshold; some Group II fibres in distal muscle nerves also contribute. Receptive field for facilitation embraces the whole limb, and the executant afferent fibres are of higher threshold. 7. Natural stimulation of the forelimb can evoke the long spinal actions, vibration or light pressure on the forepaw eliciting FDHL inhibition, and strong pinching evoking the more general facilitation. Possible functional roles of these actions in the intact animal are discussed.  (+info)

Neuronal basis of neuroleptic-induced extrapyramidal side effects. (8/33)

The article reviews presently commonly accepted concepts of neuronal basis of neuroleptic-induced extrapyramidal side effects. The data obtained both, in humans and laboratory animals, point to the blockade of a large number of the striatal dopamine D2 receptors by neuroleptics as a primary cause of these disturbances. This phenomenon leads to the appearance of parkinsonian symptoms shortly after therapy commencement. On the other hand, chronic administration of neuroleptics evokes supersensitivity to dopamine connected with the increased number of D2 receptors and supersensitivity of D1 receptors, which can be significant for the development of tardive dyskinesia. Primary and secondary changes in the function of dopamine receptors lead to partially opposite, pathological changes in the activity of neuronal pathways connecting the basal ganglia. Besides functional changes, neuroleptic-induced lesions of the striatal neurons and genetic predispositions can also play a role in tardive dyskinesia.  (+info)

Extrapyramidal tracts are a part of the motor system that lies outside of the pyramidal tracts, which are responsible for controlling voluntary movements. These extrapyramidal tracts consist of several different pathways in the brain and spinal cord that work together to regulate and coordinate involuntary movements, muscle tone, and posture.

The extrapyramidal system includes structures such as the basal ganglia, cerebellum, and brainstem, and it helps to modulate and fine-tune motor activity. Disorders of the extrapyramidal tracts can result in a variety of symptoms, including rigidity, tremors, involuntary movements, and difficulty with coordination and balance.

Some common conditions that affect the extrapyramidal system include Parkinson's disease, Huntington's disease, and drug-induced movement disorders. Treatment for these conditions may involve medications that target specific components of the extrapyramidal system to help alleviate symptoms and improve function.

Basal ganglia diseases are a group of neurological disorders that affect the function of the basal ganglia, which are clusters of nerve cells located deep within the brain. The basal ganglia play a crucial role in controlling movement and coordination. When they are damaged or degenerate, it can result in various motor symptoms such as tremors, rigidity, bradykinesia (slowness of movement), and difficulty with balance and walking.

Some examples of basal ganglia diseases include:

1. Parkinson's disease - a progressive disorder that affects movement due to the death of dopamine-producing cells in the basal ganglia.
2. Huntington's disease - an inherited neurodegenerative disorder that causes uncontrolled movements, emotional problems, and cognitive decline.
3. Dystonia - a movement disorder characterized by sustained or intermittent muscle contractions that cause twisting and repetitive movements or abnormal postures.
4. Wilson's disease - a rare genetic disorder that causes excessive copper accumulation in the liver and brain, leading to neurological and psychiatric symptoms.
5. Progressive supranuclear palsy (PSP) - a rare brain disorder that affects movement, gait, and balance, as well as speech and swallowing.
6. Corticobasal degeneration (CBD) - a rare neurological disorder characterized by progressive loss of nerve cells in the cerebral cortex and basal ganglia, leading to stiffness, rigidity, and difficulty with movement and coordination.

Treatment for basal ganglia diseases varies depending on the specific diagnosis and symptoms but may include medication, surgery, physical therapy, or a combination of these approaches.

Antipsychotic agents are a class of medications used to manage and treat psychosis, which includes symptoms such as delusions, hallucinations, paranoia, disordered thought processes, and agitated behavior. These drugs work by blocking the action of dopamine, a neurotransmitter in the brain that is believed to play a role in the development of psychotic symptoms. Antipsychotics can be broadly divided into two categories: first-generation antipsychotics (also known as typical antipsychotics) and second-generation antipsychotics (also known as atypical antipsychotics).

First-generation antipsychotics, such as chlorpromazine, haloperidol, and fluphenazine, were developed in the 1950s and have been widely used for several decades. They are generally effective in reducing positive symptoms of psychosis (such as hallucinations and delusions) but can cause significant side effects, including extrapyramidal symptoms (EPS), such as rigidity, tremors, and involuntary movements, as well as weight gain, sedation, and orthostatic hypotension.

Second-generation antipsychotics, such as clozapine, risperidone, olanzapine, quetiapine, and aripiprazole, were developed more recently and are considered to have a more favorable side effect profile than first-generation antipsychotics. They are generally effective in reducing both positive and negative symptoms of psychosis (such as apathy, anhedonia, and social withdrawal) and cause fewer EPS. However, they can still cause significant weight gain, metabolic disturbances, and sedation.

Antipsychotic agents are used to treat various psychiatric disorders, including schizophrenia, bipolar disorder, major depressive disorder with psychotic features, delusional disorder, and other conditions that involve psychosis or agitation. They can be administered orally, intramuscularly, or via long-acting injectable formulations. The choice of antipsychotic agent depends on the individual patient's needs, preferences, and response to treatment, as well as the potential for side effects. Regular monitoring of patients taking antipsychotics is essential to ensure their safety and effectiveness.

Haloperidol is an antipsychotic medication, which is primarily used to treat schizophrenia and symptoms of psychosis, such as delusions, hallucinations, paranoia, or disordered thought. It may also be used to manage Tourette's disorder, tics, agitation, aggression, and hyperactivity in children with developmental disorders.

Haloperidol works by blocking the action of dopamine, a neurotransmitter in the brain, which helps to regulate mood and behavior. It is available in various forms, including tablets, liquid, and injectable solutions. The medication can cause side effects such as drowsiness, restlessness, muscle stiffness, and uncontrolled movements. In rare cases, it may also lead to more serious neurological side effects.

As with any medication, haloperidol should be taken under the supervision of a healthcare provider, who will consider the individual's medical history, current medications, and other factors before prescribing it.

Catalepsy is a medical condition characterized by a trance-like state, with reduced sensitivity to pain and external stimuli, muscular rigidity, and fixed postures. In this state, the person's body may maintain any position in which it is placed for a long time, and there is often a decreased responsiveness to social cues or communication attempts.

Catalepsy can be a symptom of various medical conditions, including neurological disorders such as epilepsy, Parkinson's disease, or brain injuries. It can also occur in the context of mental health disorders, such as severe depression, catatonic schizophrenia, or dissociative identity disorder.

In some cases, catalepsy may be induced intentionally through hypnosis or other forms of altered consciousness practices. However, when it occurs spontaneously or as a symptom of an underlying medical condition, it can be a serious concern and requires medical evaluation and treatment.

Procyclidine is an anticholinergic medication that is primarily used to treat Parkinson's disease and related disorders. It works by blocking the action of acetylcholine, a neurotransmitter in the brain that is involved in the regulation of motor function. By doing so, procyclidine can help to reduce muscle stiffness, tremors, spasms, and other symptoms associated with Parkinson's disease.

In addition to its use in treating Parkinson's disease, procyclidine may also be used off-label to treat other conditions, such as certain types of nerve pain or side effects caused by other medications. It is important to note that procyclidine can have significant side effects, particularly at higher doses, and should only be used under the close supervision of a healthcare provider.

Drug-induced akathisia is a type of movement disorder that is a side effect of certain medications. The term "akathisia" comes from the Greek words "a-," meaning "without," and "kathisia," meaning "sitting." It is characterized by a subjective feeling of restlessness and an uncontrollable urge to be in constant motion, accompanied by objective motor symptoms such as fidgeting, rocking, or pacing.

Drug-induced akathisia is most commonly associated with the use of antipsychotic medications, particularly those that block dopamine receptors in the brain. Other drugs that have been linked to akathisia include certain antidepressants, anti-nausea medications, and some beta blockers used to treat heart conditions.

The symptoms of drug-induced akathisia can range from mild to severe and may include:

* A subjective feeling of inner restlessness or anxiety
* An uncontrollable urge to move, such as fidgeting, rocking, or pacing
* Difficulty sitting still or lying down
* Agitation and irritability
* Sleep disturbances
* Depression or dysphoria
* Suicidal thoughts or behaviors (in severe cases)

The symptoms of drug-induced akathisia can be distressing and may contribute to noncompliance with medication treatment. In some cases, the symptoms may resolve on their own after a period of time, but in other cases, they may persist or worsen, requiring a change in medication or the addition of other medications to manage the symptoms. It is important for individuals who are taking medications that have been associated with akathisia to report any new or worsening symptoms to their healthcare provider as soon as possible.

Risperidone is an atypical antipsychotic medication that is primarily used to treat certain mental/mood disorders (such as schizophrenia, bipolar disorder, and irritability associated with autistic disorder). It works by helping to restore the balance of certain natural substances in the brain. Risperidone belongs to a class of drugs called benzisoxazole derivatives.

This medication can decrease aggression and schizophrenic symptoms such as hallucinations, delusional thinking, and hostility. It may also help to improve your mood, thoughts, and behavior. Some forms of risperidone are also used for the treatment of irritability in children and adolescents with autistic disorder (a developmental disorder that affects communication and behavior).

It's important to note that this is a general medical definition, and the use of risperidone should always be under the supervision of a healthcare professional, as it can have potential side effects and risks.

Clozapine is an atypical antipsychotic medication that is primarily used to treat schizophrenia in patients who have not responded to other antipsychotic treatments. It is also used off-label for the treatment of severe aggression, suicidal ideation, and self-injurious behavior in individuals with developmental disorders.

Clozapine works by blocking dopamine receptors in the brain, particularly the D4 receptor, which is thought to be involved in the development of schizophrenia. It also has a strong affinity for serotonin receptors, which contributes to its unique therapeutic profile.

Clozapine is considered a medication of last resort due to its potential side effects, which can include agranulocytosis (a severe decrease in white blood cell count), myocarditis (inflammation of the heart muscle), seizures, orthostatic hypotension (low blood pressure upon standing), and weight gain. Because of these risks, patients taking clozapine must undergo regular monitoring of their blood counts and other vital signs.

Despite its potential side effects, clozapine is often effective in treating treatment-resistant schizophrenia and has been shown to reduce the risk of suicide in some patients. It is available in tablet and orally disintegrating tablet formulations.

Secondary Parkinson's disease, also known as acquired or symptomatic Parkinsonism, is a clinical syndrome characterized by the signs and symptoms of classic Parkinson's disease (tremor at rest, rigidity, bradykinesia, and postural instability) but caused by a known secondary cause. These causes can include various conditions such as brain injuries, infections, drugs or toxins, metabolic disorders, and vascular damage. The underlying pathology of secondary Parkinson's disease is different from that of classic Parkinson's disease, which is primarily due to the degeneration of dopamine-producing neurons in a specific area of the brain called the substantia nigra pars compacta.

Olivopontocerebellar atrophies (OPCA) are a group of rare, progressive neurodegenerative disorders that primarily affect the cerebellum, olive (inferior olivary nucleus), and pons in the brainstem. The condition is characterized by degeneration and atrophy of these specific areas, leading to various neurological symptoms.

The term "olivopontocerebellar atrophies" encompasses several subtypes, including:

1. Hereditary spastic paraplegia with cerebellar ataxia (SPG/ATA) - Autosomal dominant or recessive inheritance pattern.
2. Hereditary dentatorubral-pallidoluysian atrophy (DRPLA) - Autosomal dominant inheritance pattern.
3. Idiopathic OPCA - No known genetic cause, possibly related to environmental factors or spontaneous mutations.

Symptoms of olivopontocerebellar atrophies may include:

* Progressive cerebellar ataxia (gait and limb incoordination)
* Dysarthria (slurred speech)
* Oculomotor abnormalities (nystagmus, gaze palsy)
* Spasticity (stiffness and rigidity of muscles)
* Dysphagia (difficulty swallowing)
* Tremors or dystonia (involuntary muscle contractions)

Diagnosis typically involves a combination of clinical examination, neuroimaging studies (MRI), genetic testing, and exclusion of other possible causes. Currently, there is no cure for olivopontocerebellar atrophies, but supportive care can help manage symptoms and improve quality of life.

Cerebellar ataxia is a type of ataxia, which refers to a group of disorders that cause difficulties with coordination and movement. Cerebellar ataxia specifically involves the cerebellum, which is the part of the brain responsible for maintaining balance, coordinating muscle movements, and regulating speech and eye movements.

The symptoms of cerebellar ataxia may include:

* Unsteady gait or difficulty walking
* Poor coordination of limb movements
* Tremors or shakiness, especially in the hands
* Slurred or irregular speech
* Abnormal eye movements, such as nystagmus (rapid, involuntary movement of the eyes)
* Difficulty with fine motor tasks, such as writing or buttoning a shirt

Cerebellar ataxia can be caused by a variety of underlying conditions, including:

* Genetic disorders, such as spinocerebellar ataxia or Friedreich's ataxia
* Brain injury or trauma
* Stroke or brain hemorrhage
* Infections, such as meningitis or encephalitis
* Exposure to toxins, such as alcohol or certain medications
* Tumors or other growths in the brain

Treatment for cerebellar ataxia depends on the underlying cause. In some cases, there may be no cure, and treatment is focused on managing symptoms and improving quality of life. Physical therapy, occupational therapy, and speech therapy can help improve coordination, balance, and communication skills. Medications may also be used to treat specific symptoms, such as tremors or muscle spasticity. In some cases, surgery may be recommended to remove tumors or repair damage to the brain.

Spinocerebellar degenerations (SCDs) are a group of genetic disorders that primarily affect the cerebellum, the part of the brain responsible for coordinating muscle movements, and the spinal cord. These conditions are characterized by progressive degeneration or loss of nerve cells in the cerebellum and/or spinal cord, leading to various neurological symptoms.

SCDs are often inherited in an autosomal dominant manner, meaning that only one copy of the altered gene from either parent is enough to cause the disorder. The most common type of SCD is spinocerebellar ataxia (SCA), which includes several subtypes (SCA1, SCA2, SCA3, etc.) differentiated by their genetic causes and specific clinical features.

Symptoms of spinocerebellar degenerations may include:

1. Progressive ataxia (loss of coordination and balance)
2. Dysarthria (speech difficulty)
3. Nystagmus (involuntary eye movements)
4. Oculomotor abnormalities (problems with eye movement control)
5. Tremors or other involuntary muscle movements
6. Muscle weakness and spasticity
7. Sensory disturbances, such as numbness or tingling sensations
8. Dysphagia (difficulty swallowing)
9. Cognitive impairment in some cases

The age of onset, severity, and progression of symptoms can vary significantly among different SCD subtypes and individuals. Currently, there is no cure for spinocerebellar degenerations, but various supportive treatments and therapies can help manage symptoms and improve quality of life.

Striatonigral degeneration (SND) is a type of neurodegenerative disorder that affects the basal ganglia, specifically the striatum and the substantia nigra. It is also known as "striatonigral degeneration with olivopontocerebellar atrophy" or "multiple system atrophy-parkinsonian type (MSA-P)".

SND is characterized by the progressive loss of nerve cells in the striatum, which receives input from the cerebral cortex and sends output to the substantia nigra. This results in a decrease in the neurotransmitter dopamine, leading to symptoms similar to those seen in Parkinson's disease (PD), such as stiffness, slowness of movement, rigidity, and tremors.

However, unlike PD, SND is also associated with degeneration of the olivopontocerebellar system, which can lead to additional symptoms such as ataxia, dysarthria, and oculomotor abnormalities. The exact cause of striatonigral degeneration is unknown, but it is believed to involve a combination of genetic and environmental factors. Currently, there is no cure for the condition, and treatment is focused on managing the symptoms.

Dysarthria is a motor speech disorder that results from damage to the nervous system, particularly the brainstem or cerebellum. It affects the muscles used for speaking, causing slurred, slow, or difficult speech. The specific symptoms can vary depending on the underlying cause and the extent of nerve damage. Treatment typically involves speech therapy to improve communication abilities.

Multiple System Atrophy (MSA) is a rare, progressive neurodegenerative disorder that affects multiple systems in the body. It is characterized by a combination of symptoms including Parkinsonism (such as stiffness, slowness of movement, and tremors), cerebellar ataxia (lack of muscle coordination), autonomic dysfunction (problems with the autonomic nervous system which controls involuntary actions like heart rate, blood pressure, sweating, and digestion), and pyramidal signs (abnormalities in the corticospinal tracts that control voluntary movements).

The disorder is caused by the degeneration of nerve cells in various parts of the brain and spinal cord, leading to a loss of function in these areas. The exact cause of MSA is unknown, but it is thought to involve a combination of genetic and environmental factors. There is currently no cure for MSA, and treatment is focused on managing symptoms and improving quality of life.

Extrapyramidal Tracts* Actions. * Search in PubMed * Search in MeSH * Add to Search ... Progressive extra-pyramidal disorder in 2 young brothers. Remarkable effects of treatment with L-dopa] [Article in French] ... Progressive extra-pyramidal disorder in 2 young brothers. Remarkable effects of treatment with L-dopa] [Article in French] ... ON THE DIAGNOSIS AND DIFFERENTIAL DIAGNOSIS OF CEREBRAL POLIOMYELITIS WITH PYRAMIDAL AND EXTRAPYRAMIDAL DISORDERS]. HUFFMANN G. ...
Pyramidal tract and extra pyramidal tracts by Pyramidal tract and extra pyramidal tractsYogesh Ramasamy. 76.3K. views•48 slides ... Pyramidal tract and extra pyramidal tracts by Yogesh Ramasamy. Pyramidal tract and extra pyramidal tracts. Yogesh Ramasamy•76.3 ... Controls glandular and cardiac function and smooth muscle such as that found in the digestive tract. There are two components: ...
In patients in whom the infection progresses to lower respiratory tract disease, the original symptoms persist, with a ... M. pneumoniae causes infections leading to clinically apparent disease involving the upper respiratory tract. In 5-10% of ... Dysfunction of the pyramidal or extrapyramidal tract. *. Cerebellar dysfunction. *. Cerebral infarction. *. Guillain-Barré ...
... along with other extra-pyramidal tracts including the vestibulospinal, tectospinal, and reticulospinal tracts. The tract is ... The rubrospinal tract is a part of the nervous system. It is a part of the lateral indirect extra-pyramidal tract. In the ... the rubrospinal tract can assume almost all the duties of the corticospinal tract when the corticospinal tract is lesioned.[ ... coursing adjacent to the lateral corticospinal tract. In humans, the rubrospinal tract is one of several major motor control ...
Rare parkinsonian syndrome and other extrapyramidal tract symptoms; dizziness; headache; paradoxical anxiety; depression; ... Reserpine is excreted in maternal breast milk, and increased respiratory tract secretions, nasal congestion, cyanosis, and ... Reserpine crosses the placental barrier, and increased respiratory tract secretions, nasal congestion, cyanosis, and anorexia ...
... is a neurodegenerative syndrome characterized by prominent cerebellar and extrapyramidal signs, dysarthria, and dysphagia. ... myelin loss in spinocerebellar tracts, posterior columns, and corticospinal tracts; gait and limb ataxia, intention tremor, ... Congenital microcephaly, extrapyramidal findings, epilepsy; autopsy in one case showed that the olivopontocerebellar system was ... myelin loss in spinocerebellar tracts, posterior columns, and corticospinal tracts; gait and limb ataxia, intention tremor, ...
This distribution includes the primary and secondary motor cortices, the pyramidal and extrapyramidal tracts, and the ... This last finding also has been observed in the anterior horn cells and pyramidal tracts. Motor neuron disease tends to occur ... The globus pallidus, caudate nucleus, corticospinal tracts, anterior horn cells of the cord, dentate nucleus, and vestibular ... Pyramidal tract signs not explained by previous stroke or spinal cord lesions ...
... which often affect the extrapyramidal nerve tracts (which control such things as muscular rigidity, painful muscle spasms, ... The first of the new class, clozapine (Clozaril), is not associated with extrapyramidal side effects, but it can produce other ...
Pyramidal and extrapyramidal tract signs manifest early in the course of disease. In the first decade of life, individuals ...
Extrapyramidal tract structure (body structure). Code System Preferred Concept Name. Extrapyramidal tract structure (body ... Extrapyramidal tract structure (body structure) {87516006 , SNOMED-CT } Parent/Child (Relationship Type) Entire extrapyramidal ... Extrapyramidal system structure (body structure) {76375004 , SNOMED-CT } Midbrain tract (body structure) {360475006 , SNOMED-CT ... tract (body structure) {362400005 , SNOMED-CT } Structure of reticulospinal tract of pons (body structure) {87086009 , SNOMED- ...
Extrapyramidal Tracts Preferred Concept UI. M0008071. Scope Note. Uncrossed tracts of motor nerves from the brain to the ... Extrapyramidal Tracts Preferred Term Term UI T015656. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1966). ... Extrapyramidal Tracts. Tree Number(s). A08.186.854.253. A08.612.380.239. Unique ID. D005116. RDF Unique Identifier. http://id. ... Uncrossed tracts of motor nerves from the brain to the anterior horns of the spinal cord, involved in reflexes, locomotion, ...
Extrapyramidal Tracts Preferred Concept UI. M0008071. Scope Note. Uncrossed tracts of motor nerves from the brain to the ... Extrapyramidal Tracts Preferred Term Term UI T015656. Date01/01/1999. LexicalTag NON. ThesaurusID NLM (1966). ... Extrapyramidal Tracts. Tree Number(s). A08.186.854.253. A08.612.380.239. Unique ID. D005116. RDF Unique Identifier. http://id. ... Uncrossed tracts of motor nerves from the brain to the anterior horns of the spinal cord, involved in reflexes, locomotion, ...
Descending tracts Extra pyramidal tracts Physiology Lecture Slideshow Jul 19, 2023 sabkuchonline.pk ... These fibers form the optic tracts. Optic Tract. *Extends from optic chiasm to the lateral geniculate nucleus. of the thalamus ... Relays visual information from the optic tract to the visual cortex via. optic radiations. Transmits point-to-point ... Optic tract fibers terminate primarily in the lateral geniculate. nucleus of the thalamus ...
2) Corticobulbar tracts - supplies the head and neck.. Extrapyramidal tracts - These tracts originate in the brain stem, ... Pyramidal and Extrapyramidal. Pyramidal tracts - These tracts originate in the cerebral cortex, carrying motor fibres to the ... Anterior spinothalamic tract - carries the sensory modalities of crude touch and pressure.. - Lateral spinothalamic tract - ... The ascending tracts refer to the neural pathways by which sensory information from the peripheral nerves is transmitted to the ...
No paralysis, cerebellar ataxia, pyramidal or extrapyramidal tract symptoms, visual disturbance, hearing loss, dysarthria, or ...
Corticobulbar and extrapyramidal tracts. Insula. Lesion laterality. Screening for Dysphagia in Acute Stroke Patients. ... The spinothalamic tract. The medullary tracts. The cerebral cortex. What Is Known About the Pathophysiology of CPSP. Treatments ...
extrapyramidové dráhy Extrapyramidal Tracts Form, Genre. vysokoškolská skripta college textbooks Conspect. 616 - Patologie. ... poruchy extrapyramidového systému extrapyramidal disorders * syndromy syndromes MeSH. ...
... wave I from extrapyramidal tracts, wave II from the ventral corticospinal tract, and wave III from the dorsal corticospinal ... wave I from extrapyramidal tracts, wave II from the ventral corticospinal tract, and wave III from the dorsal corticospinal ... wave I from extrapyramidal tracts, wave II from the ventral corticospinal tract, and wave III from the dorsal corticospinal ... wave I from extrapyramidal tracts, wave II from the ventral corticospinal tract, and wave III from the dorsal corticospinal ...
Spasticity is related to damage of pyramidal tracts, and Rigidity causes the damage of extrapyramidal tracts. Muscle pain is ... Spasticity occurs in pyramidal tract lesions, whereas Rigidity occurs in extrapyramidal tracts. *Spasticity happens with ... It is seen in extrapyramidal tracts.. It refers to a state of deformity under pressure. Muscle pain is caused by rigidity. ... It is seen in extrapyramidal tracts. It refers to a state of deformity under pressure. There is a disease called Parkinsons ...
Other symptoms of PKU include tremors and pyramidal tract signs, increased muscle tone and hyperreflexia with 5% of patients ... developing spastic paraparesis (Berg, 1994). Extrapyramidal signs such as choreoathetosis have also been described (Thompson et ...
The corticobulbar tracts from the upper face cross and recross en route to the pons; the tracts to the lower face cross only ... Extrapyramidal system. The extrapyramidal system consists of the basal nuclei and the descending motor projections other than ... Discharges from the facial motor area are carried through fascicles of the corticobulbar tract to the internal capsule, then ... The masked facies associated with Parkinsonism are known to be the result of destruction of the extrapyramidal pathways. The ...
... descending and intersegmental tracts. Ascending tracts are formed of primary afferent fibers which enter through posterior ... Extrapyramidal tracts begin within the brainstem and carry motor fibers to the spinal cord. They include the tectospinal tract ... medial reticulospinal tract, vestibulospinal tract, lateral reticulospinal tract and the rubrospinal tract. Pyramidal tracts ... while extrapyramidal tracts are responsible for the involuntary and automatic control.Intersegmental tracts are short ascending ...
Synonym: Pyramidal Tract Signs. Abnormality of Extrapyramidal Motor Function. Synonym: Extrapyramidal Dysfunction ... Functional neurological abnormalities related to dysfunction of the pyramidal tract.. Functional neurological abnormalities ...
Spiral saphenous vein just above the basal ganglia or extrapyramidal tracts and fistulas bladder or bowel obstruction. Sedation ...
... projections and diffusion tensor imaging of the intracranial pyramidal and extrapyramidal tracts. Brain Structure and Function. ... projections and diffusion tensor imaging of the intracranial pyramidal and extrapyramidal tracts. Peruffo, A., Corain, L., ...
So thats what happens if the basal ganglia or the extrapyramidal tracts are impaired or damaged, or affected in some way. And ... So when the basal ganglia or these extrapyramidal tracts are damaged or under-developed or impaired in someone with cerebral ... so we call these tracts extrapyramidal because they do not go through the medullary pyramids on their way to the spinal cord. ... they use these highways of neurons called the extrapyramidal tracts to send messages to other structures in the brain that ...
... slower progression and speech and psychiatric disorders along with the extrapyramidal and corticospinal tract features of the ... Two developed atrophy of the distal muscles, and 1 experienced corticospinal tract impairment. Each girl of a pair of twins ... As a result of disturbance of supranuclear corticospinal tract function, drooling may become a difficult problem. Small doses ... The corroborative features are corticospinal tract involvement-spasticity or extensor toe signs, progressive intellectual ...
Anterior and lateral corticospinal tracts and also corticonuclear tract belong to pyramidal pathways. The extrapyramidal tracts ... Anterior spinocerebellar tract (Gowers tract). Two-neurons way. This tract differs from previous by its second neuron, a body ... Diagram of the tracts in the internal capsule. Motor tract red. The sensory tract (blue) is not direct, but formed of neurons ... Spinocerebellar tracts (Flechsig and Gowers tracts) are the ascending links for this regulation. Spinocerebellar tracts send ...

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