The most effective treatment of astasia seems to be a removal of stress inducing stimuli and allowing the patient to rest and regain strength. Despite the lack of a direct prescribable cure for the effect of astasia on the motor system of the legs, in almost all documented cases physical rehabilitation and relief from mental stressors have led to a full recovery. Although astasia is not expressly associated with any neurological disorders, there is a strong correlation between general mental hysteria and the symptoms of astasia. Therefore, isolation of the patient from the situation causing them hysteria is the most efficient way to rid them of disabling motor symptoms. Another method for treatment that patients who experience astasia is to have therapy for the triceps surae muscle. This therapy can help strengthen these muscles to help maintain an upright posture. It has also been suggested that ankle-foot orthoses be prescribed for these patients. This would help patients with astasia maintain balance by preventing ankle dorsiflexion.

Currently, physical therapy and rehabilitation are widely accepted as the best treatments for the symptoms of astasia. There is, however, evidence to suggest that regulation of a patient's social situation and behavioral influences can influence the effectiveness of rehabilitation. A 1975 study shows that when a patient is given direct encouragement and social distractions their physical recovery proceeds much faster than when only basic instructions are provided to them.

Most current treatments for aboulia are pharmacological, including the use of antidepressants. However, antidepressant treatment is not always successful and this has opened the door to alternative methods of treatment. The first step to successful treatment of aboulia, or any other DDM, is a preliminary evaluation of the patient's general medical condition and fixing the problems that can be fixed easily. This may mean controlling seizures or headaches, arranging physical or cognitive rehabilitation for cognitive and sensorimotor loss, or ensuring optimal hearing, vision, and speech. These elementary steps also increase motivation because improved physical status may enhance functional capacity, drive, and energy and thereby increase the patient's expectation that initiative and effort will be successful.

There are 5 steps to pharmacological treatment:

1. Optimize medical status.

2. Diagnose and treat other conditions more specifically associated with diminished motivation (e.g., apathetic hyperthyroidism, Parkinson's disease).

3. Eliminate or reduce doses of psychotropics and other agents that aggravate motivational loss (e.g., SSRIs, dopamine antagonists).

4. Treat depression efficaciously when both DDM and depression are present.

5. Increase motivation through use of stimulants, dopamine agonists, or other agents such as cholinesterase inhibitors.

Binswanger's disease has no cure and has been shown to be the most severe impairment of all of the vascular dementias. The best way to manage the vascular risk factors that contribute to poor perfusion in the brain is to treat the cause, such as chronic hypertension or diabetes. It has been shown that current Alzheimer’s medication, donepezil (trade name Aricept), may help Binswanger’s Disease patients as well . Donepezil increases the acetylcholine in the brain through a choline esterase inhibitor which deactivates the enzyme that breaks down acetylcholine. Alzheimer as well as Binswanger patients have low levels of acetylcholine and this helps to restore the normal levels of neurotransmitters in the brain. This drug may improve memory, awareness, and the ability to function. If no medical interception of the disease is performed then the disease will continue to worsen as the patient ages due to the continuing atrophy of the white matter from whatever was its original cause.

Blocq's disease was first considered by Paul Blocq (1860–1896), who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra.

In the third paper published by Paul Blocq, he was trying to determine the neurophysiology behind this disease by relating the cerebral cortex (the decision making) and the spinal cord (the decision executer). His hypothesis was that there would exist an inhibitory influence which exerted and influenced the cortical or spinal centers for standing and walking.

The treatment to battle the disease chorea-acanthocytosis is completely symptomatic. For example, Botulinum toxin injections can help to control orolingual dystonia.

Deep Brain Stimulation is a treatment that has varied effects on the people suffering from the symptoms of this disease, for some it has helped in a large way and for other people it did not help whatsoever, it is more effective on specific symptoms of the disease. Patients with chorea-acanthocytosis should undergo a cardiac evaluation every 5 years to look for cardiomyopathy.

The doctor will review the person's medical history and perform a complete physical and neurological examination that will include an evaluation of the gait. The doctor may ask the patient to walk in a corridor or climb stairs to observe specific features including:

1. Stance, posture, and base (wide or narrow).

2. Gait initiation (including start hesitation or freezing).

3. Walking speed, stride length, step height, foot clearance.

4. Continuity, symmetry, trunk sway, path deviation, arm swing.

5. Involuntary movements.

6. Ability to turn.

7. Ability to rise from a chair (without using the arms).

8. Chair Testing: Each patient was asked to walk 20–30 feet forward and backward toward the examiner. Patients were then asked to sit in a swivel chair with wheels and to propel the chair forward and backward.

""Astasia" redirects here. This term was also applied to chlorophyll-less "Euglena.

Astasis is a lack of motor coordination marked by an inability to stand, walk or even sit without assistance due to disruption of muscle coordination.

The term "astasia" is interchangeable with "astasis" and is most commonly referred to as "astasia" in the literature describing it. Astasis is the inability to stand or sit up without assistance in the absence of motor weakness or sensory loss (although the inclusion of 'the lack of motor weakness' has been debated by some physicians). It is categorized more as a symptom than an actual disease, as it describes a disruption of muscle coordination resulting in this deficit. The disturbance differs from cerebellar ataxia in that with astasis the gait can be relatively normal, with balance significantly impaired during transition from a seated to standing position. This balance impairment is similar to patients with vestibulocerebellar syndrome, which is a progressive neurological disease with many symptoms and effects.

Astasis has been seen in patients with diverse thalamic lesions, predominantly affecting the posterior lateral region of the brain. It is most frequently accompanied by abasia, although not always. Abasia is a symptom very similar to it and is the inability to walk. The two are most commonly seen in astasia-abasia, which is also called Blocq's disease. It is more common for astasia and abasia to be seen together than it is to see either one or the other.

Batten disease is a terminal illness; the FDA has approved Brineura (cerliponase alfa) as a treatment for a specific form of Batten disease. Brineura is the first FDA-approved treatment to slow loss of walking ability (ambulation) in symptomatic pediatric patients 3 years of age and older with late infantile neuronal ceroid lipofuscinosis type 2 (CLN2), also known as tripeptidyl peptidase-1 (TPP1) deficiency. Palliative treatment is symptomatic and supportive.

Aboulia or abulia (from , meaning "will", with the prefix -a), in neurology, refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM). Aboulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than aboulia. A patient with aboulia is unable to act or make decisions independently. It may range in severity from subtle to overwhelming. It is also known as Blocq's disease (which also refers to abasia and astasia-abasia). Aboulia was originally considered to be a disorder of the will.

Surgical excision of fatty tissue deposits around joints (liposuction) has been used in some cases. It may temporarily relieve symptoms although recurrences often develop.

Traditional analgesics

The pain in Dercum's disease is often reported to be refractory to analgesics and to non-steroidal anti-inflammatory drugs (NSAIDs). However, this has been contradicted by the findings of Herbst et al. They reported that the pain diminished in 89% of patients (n=89) when treated with NSAIDs and in 97% of patients when treated with narcotic analgesics (n=37). The dosage required and the duration of the pain relief are not precisely stated in the article.

Lidocaine

An early report from 1934 showed that intralesional injections of procaine (Novocain®) relieved pain in six cases. More recently, other types of local treatment of painful sites with lidocaine patches (5%) (Lidoderm®) or lidocaine/prilocaine (25 mg/25 mg) cream (EMLA®) have shown a reduction of pain in a few cases.

In the 1980s, treatment with intravenous infusions of lidocaine (Xylocaine®) in varying doses was reported in nine patients. The resulting pain relief lasted from 10 hours to 12 months. In five of the cases, the lidocaine treatment was combined with mexiletine (Mexitil®), which is a class 1B anti-arrhythmic with similar pharmacological properties as lidocaine.

The mechanism by which lidocaine reduces pain in Dercum's disease is unclear. It may block impulse conduction in peripheral nerves, and thereby disconnect abnormal nervous impulse circuits. Nonetheless, it might also depress cerebral activity that could lead to increased pain thresholds. Iwane et al. performed an EEG during the administration of intravenous lidocaine. The EEG showed slow waves appearing 7 minutes after the start of the infusion and disappearing within 20 minutes after the end of the infusion. On the other hand, the pain relief effect was the greatest at about 20 minutes after the end of the infusion.

Based on this, the authors concluded that the effect of lidocaine on peripheral nerves most likely explains why the drug has an effect on pain in Dercum's disease. In contrast, Atkinson et al. have suggested that an effect on the central nervous system is more likely, as lidocaine can depress consciousness and decrease cerebral metabolism. In addition, Skagen et al. demonstrated that a patient with Dercum's disease lacked the vasoconstrictor response to arm and leg lowering, which indicated that the sympathicusmediated local veno-arteriolar reflex was absent. This could suggest increased sympathetic activity. An infusion of lidocaine increased blood flow in subcutaneous tissue and normalised the vasoconstrictor response when the limbs were lowered. The authors suggested that the pain relief was caused by a normalisation of up-regulated sympathetic activity.

Methotrexate and infliximab

One patient's symptoms were improved with methotrexate and infliximab. However, in another patient with Dercum's disease, the effect of methotrexate was discreet. The mechanism of action is unclear. Previously, methotrexate has been shown to reduce neuropathic pain caused by peripheral nerve injury in a study on rats. The mechanism in the rat study case was thought to be a decrease in microglial activation subsequent to nerve injury. Furthermore, a study has shown that infliximab reduces neuropathic pain in patients with central nervous system sarcoidosis. The mechanism is thought to be mediated by tumour necrosis factor inhibition.

Interferon α-2b

Two patients were successfully treated with interferon α-2b. The authors speculated on whether the mechanism could be the antiviral effect of the drug, the production of endogenous substances, such as endorphins, or interference with the production of interleukin-1 and tumour necrosis factor. Interleukin-1 and tumour necrosis factor are involved in cutaneous hyperalgesia.

Corticosteroids

A few patients noted some improvement when treated with systemic corticosteroids (prednisolone), whereas others experienced worsening of the pain. Weinberg et al. treated two patients with juxta-articular Dercum's disease with intralesional injections of methylprednisolone (Depo-Medrol). The patients experienced a dramatic improvement.

The mechanism for the pain-reducing ability of corticosteroids in some conditions is unknown. One theory is that they inhibit the effects of substances, such as histamine, serotonin, bradykinin, and prostaglandins. As the aetiology of Dercum's disease is probably not inflammatory, it is plausible that the improvement some of the patients experience when using corticosteroids is not caused by an anti-inflammatory effect.

The twins require the use of wheelchairs for mobility and are unable to speak without the assistance of electronic speaking aids. They experience persistent and painful muscle spasms which are worsened by emotional distress. They are currently living with their parents, with the assistance of hospice workers. Doctors continue to administer tests to the twins in search of a treatment.

In June 1987, a phase-I clinical trial was launched at Weill Cornell Medical College of Cornell University to study a gene therapy method for treatment of the signs and symptoms of LINCL. The experimental drug works by delivering a gene transfer vector called AAV2CUhCLN2 to the brain. Although the trial is not matched, randomized, or blinded and lacked a contemporaneous placebo/sham control group, assessment of the primary outcome variable suggests a slowing of progression of LINCL in the treated children.

Researchers believe the neurological deficits common in JNCL could be due to overactive AMPA receptors in the cerebellum. To test this hypothesis, researchers administered AMPA antagonist drugs into affected mice. The motor skills of the affected mice showed significant improvement after the antagonist treatment, which supported the hypothesis that the neurological deficits in JNCL are due to overactive AMPA receptors. This research could eventually help to alleviate neurological deficits of JNCL in humans.

In November 2006, after receiving FDA clearance, neurosurgeon Nathan Selden, pediatrician Bob Steiner, and colleagues at Doernbecher Children's Hospital at Oregon Health and Science University began a clinical study in which purified neural stem cells were injected into the brain of Daniel Kerner, a six-year-old child with Batten disease, who had lost the ability to walk and talk. This patient was the first of six to receive the injection of a stem cell product from StemCells Inc., a Palo Alto biotech company. These are believed to be the first-ever transplants of fetal stem cells into the human brain. By early December, the child had recovered well enough to return home, and some signs of speech returning were reported. Daniel Kerner died on April 12, 2010. The main goal of phase-I clinical trials, however, was to investigate the safety of transplantation. Overall, the phase-I data demonstrated that high doses of human neural stem cells, delivered by a direct transplantation procedure into multiple sites within the brain, followed by 12 months of immunosuppression, were well tolerated by all six patients enrolled in the trial. The patients’ medical, neurological, and neuropsychological conditions, following transplantation, appeared consistent with the normal course of the disease.

Mycophenolate mofetil is being tested to determine its ability to safely slow or halt neurodegeneration. A non-randomised safety and efficacy trial of a gene transfer vector is underway.

Binswanger's disease, also known as subcortical leukoencephalopathy, is a form of small vessel vascular dementia caused by damage to the white brain matter. White matter atrophy can be caused by many circumstances including chronic hypertension as well as old age. This disease is characterized by loss of memory and intellectual function and by changes in mood. These changes encompass what are known as executive functions of the brain. It usually presents between 54 and 66 years of age, and the first symptoms are usually mental deterioration or stroke.

It was described by Otto Binswanger in 1894, and Alois Alzheimer first used the phrase "Binswanger's disease" in 1902. However, Olszewski is credited with much of the modern-day investigation of this disease which began in 1962.

Currently, there is no cure for Urbach–Wiethe disease although there are some ways to individually treat many of its symptoms. There has been some success with oral dimethyl sulfoxide (DMSO) and intralesional heparin, but this is not true in all cases. D-penicillamine has also shown promise, but has yet to have been used extensively. There are also some reports of patients being treated with etretinate, a drug typically prescribed to treat psoriasis. In some cases, calcifications in the brain can lead to abnormal electrical activity among neurons. Some patients are given anti-seizure medication to help deal with these abnormalities. Tracheostomy is often used to relieve upper respiratory tract infections. Carbon dioxide laser surgery of thickened vocal cords and beaded eyelid papules have improved these symptoms for patients. The discovery of the mutations of the ECM1 gene has opened the possibility of gene therapy or a recombinant EMC1 protein for Urbach–Wiethe disease treatment, but neither of these two options are currently available.

Currently Sandhoff disease does not have any standard treatment and does not have a cure. However, a person suffering from the disease needs proper nutrition, hydration, and maintenance of clear airways. To reduce some symptoms that may occur with Sandhoff disease, the patient may take anticonvulsants to manage seizures or medications to treat respiratory infections, and consume a precise diet consisting of puree foods due to difficulties swallowing. Infants with the disease usually die by the age of 3 due to respiratory infections. The patient must be under constant surveillance because they can suffer from aspiration or lack the ability to change from the passageway to their lungs versus their stomach and their spit travels to the lungs causing bronchopneumonia. The patient also lacks the ability to cough and therefore must undergo a treatment to shake up their body to remove the mucus from the lining of their lungs. Medication is also given to patients to lessen their symptoms including seizures.

Currently the government is testing several treatments including N-butyl-deoxynojirimycin in mice, as well as stem cell treatment in humans and other medical treatments recruiting test patients.

Although there is no known cure for Krabbe disease, bone marrow transplantation has been shown to benefit cases early in the course of the disease. Generally, treatment for the disorder is symptomatic and supportive. Physical therapy may help maintain or increase muscle tone and circulation. Cord blood transplants have been successful in stopping the disease as long as they are given before overt symptoms appear.

Urbach–Wiethe disease is typically not a life-threatening condition. The life expectancy of these patients is normal as long as the potential side effects of thickening mucosa, such as respiratory obstruction, are properly addressed. Although this may require a tracheostomy or carbon dioxide laser surgery, such steps can help ensure that individuals with Urbach–Wiethe disease are able to live a full life. Oral dimethyl sulfoxide (DMSO) has been shown to reduce skin lesions, helping to minimize discomfort for these individuals.

Pick's disease is a term that can be used in two different ways. It has traditionally been used as a term for a group of neurodegenerative diseases with symptoms attributable to frontal and temporal lobe dysfunction. Common symptoms that are noticed early are personality and emotional changes, as well as deterioration of language. This condition is now more commonly called frontotemporal dementia by professionals, and the use of "Pick's disease" as a clinical diagnosis has fallen out of fashion. The second use of the term (and the one now used among professionals) is to mean a specific pathology that is one of the causes of frontotemporal lobar degeneration. These two uses have previously led to confusion among professionals and patients and so its use should be restricted to the specific pathological subtype described below. It is also known as Pick disease and PiD (not to be confused with pelvic inflammatory disease (PID) or Parkinson's disease (PD)). A defining characteristic of the disease is build-up of tau proteins in neurons, accumulating into silver-staining, spherical aggregations known as "Pick bodies".

The first treatment for Fabry's disease was approved by the US FDA on April 24, 2003. Fabrazyme (agalsidase beta, or Alpha-galactosidase) was licensed to the Genzyme Corporation. It is an enzyme replacement therapy (ERT) designed to provide the enzyme the patient is missing as a result of a genetic malfunction. The drug is expensive — in 2012, Fabrazyme's annual cost was about US$200,000 per patient, which is unaffordable to many patients around the world without enough insurance. ERT is not a cure, but can allow improved metabolism and partially prevent disease progression, as well as potentially reverse some symptoms.

The pharmaceutical company Shire manufactures agalsidase alpha (which differs in the structure of its oligosaccharide side chains) under the brand name Replagal as a treatment for Fabry's disease, and was granted marketing approval in the EU in 2001. FDA approval was applied for the United States. However, Shire withdrew their application for approval in the United States in 2012, citing that the agency will require additional clinical trials before approval.

Clinically the two products are generally perceived to be similar in effectiveness. Both are available in Europe and in many other parts of the world, but treatment costs remain very high.

Besides these drugs, a gene therapy treatment is also available from the Canadian Institutes of Health. Other treatments (oral chaperone therapy -Amicus-, plant-based ERT -Protalix-, substrate reduction therapy -Sanofi-Genzyme-, bio-better ERT -Codexis-, gene editing solution -Sangamo- are currently being researched.

Pain associated with Fabry disease may be partially alleviated by ERT in some patients, but pain management regimens may also include analgesics, anticonvulsants, and nonsteroidal anti-inflammatory drugs, though the latter are usually best avoided in renal disease.

Chorea-acanthocytosis (ChAc, also called Choreoacanthocytosis), is a rare hereditary disease caused by a mutation of the gene that directs structural proteins in red blood cells. It belongs to a group of four diseases characterized under the name Neuroacanthocytosis. When a patient's blood is viewed under a microscope, some of the red blood cells appear thorny. These thorny cells are called acanthocytes.

Other effects of the disease may include epilepsy, behaviour changes, muscle degeneration, and neuronal degradation similar to Huntington's Disease. The average age of onset of symptoms is 35 years. The disease is incurable and inevitably leads to premature death.

Some more information about Chorea-acanthocytosis is that it is a very complex autosomal recessive adult-onset neurodegenerative disorder. It often shows itself as a mixed movement disorder, in which chorea, tics, dystonia and even parkinsonism may appear as a symptom.

This disease is also characterized by the presence of a few different movement disorders including chorea, dystonia etc.

Chorea-acanthocytosis is considered an autosomal recessive disorder, although a few cases with autosomal dominant inheritance have been noted.

Adult-onset Still's disease is treated with anti-inflammatory drugs. Steroids such as prednisone are used to treat severe symptoms of Still's. Other commonly used medications include hydroxychloroquine, penicillamine, azathioprine, methotrexate, etanercept, anakinra, cyclophosphamide, adalimumab, rituximab, and infliximab.

Newer drugs target interleukin-1 (IL-1), particularly IL-1β. A randomized, multicenter trial reported better outcomes in a group of 12 patients treated with anakinra than in a group of 10 patients taking other disease-modifying antirheumatic drugs. Other anti-IL1β drugs are being developed, including canakinumab and rilonacept.

The condition "juvenile-onset Still's disease" is now usually grouped under juvenile rheumatoid arthritis. However, there is some evidence that the two conditions are closely related.

No cures for lysosomal storage diseases are known, and treatment is mostly symptomatic, although bone marrow transplantation and enzyme replacement therapy (ERT) have been tried with some success. ERT can minimize symptoms and prevent permanent damage to the body. In addition, umbilical cord blood transplantation is being performed at specialized centers for a number of these diseases. In addition, substrate reduction therapy, a method used to decrease the production of storage material, is currently being evaluated for some of these diseases. Furthermore, chaperone therapy, a technique used to stabilize the defective enzymes produced by patients, is being examined for certain of these disorders. The experimental technique of gene therapy may offer cures in the future.

Ambroxol has recently been shown to increase activity of the lysosomal enzyme glucocerebrosidase, so it may be a useful therapeutic agent for both Gaucher disease and Parkinson's disease. Ambroxol triggers the secretion of lysosomes from cells by inducing a pH-dependent calcium release from acidic calcium stores. Hence, relieving the cell from accumulating degradation products is a proposed mechanism by which this drug may help.

Since phytanic acid is not produced in the human body, individuals with Refsum disease are commonly placed on a phytanic acid-restricted diet and avoid the consumption of fats from ruminant animals and certain fish, such as tuna, cod, and haddock. Grass feeding animals and their milk are also avoided. Recent research has shown that CYP4 isoform enzymes could help reduce the over-accumulation of phytanic acid "in vivo". Plasmapheresis is another medical intervention used to treat patients. This involves the filtering of blood to ensure there is no accumulation of phytanic acid.

There is no way to reverse VHL mutations, but early recognition and treatment of specific manifestations of VHL can substantially decrease complications and improve quality of life. For this reason, individuals with VHL disease are usually screened routinely for retinal angiomas, CNS hemangioblastomas, clear-cell renal carcinomas and pheochromocytomas. CNS hemangioblastomas are usually surgically removed if they are symptomatic. Photocoagulation and cryotherapy are usually used for the treatment of symptomatic retinal angiomas, although anti-angiogenic treatments may also be an option. Renal tumours may be removed by a partial nephrectomy or other techniques such as radiofrequency ablation.