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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.
Sedative drugs are often prescribed for vertigo and dizziness, but these usually treat the symptoms rather than the underlying cause. Lorazepam (Ativan) is often used and is a sedative which has no effect on the disease process, but rather helps patients cope with the sensation.
Anti-nauseants, like those prescribed for motion sickness, are also often prescribed but do not affect the prognosis of the disorder.
Specifically for Meniere's disease a medication called Serc (Beta-histine) is available. There is some evidence to support its effectiveness in reducing the frequency of attacks. Also Diuretics, like Diazide (HCTZ/triamterene), are effective in many patients. Finally, ototoxic medications delivered either systemically or through the eardrum can eliminate the vertigo associated with Meniere's in many cases, although there is about a 10% risk of further hearing loss when using ototoxic medications.
Treatment is specific for underlying disorder of balance disorder:
- anticholinergics
- antihistamines
- benzodiazepines
- calcium channel antagonists, specifically Verapamil and Nimodipine
- GABA modulators, specifically gabapentin and baclofen
- Neurotransmitter reuptake inhibitors such as SSRIs, SNRIs and Tricyclics
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.
Treatment includes balance retraining exercises (vestibular rehabilitation). The exercises include movements of the head and body specifically developed for the patient. This form of therapy is thought to promote habituation, adaptation of the vestibulo-ocular reflex, and/or sensory substitution. Vestibular retraining programs are administered by professionals with knowledge and understanding of the vestibular system and its relationship with other systems in the body.
Patients with dementia who are confined to a nursing home and may have undiagnosed NPH can possibly become independent again once treated. So far only one study was able to evaluate the prevalence of NPH, both diagnosed and undiagnosed, among residents of assisted-living facilities, showing a prevalence in 9 to 14% of the residents.
NPH may be relieved by surgically implanting a ventriculoperitoneal shunt to drain excess cerebrospinal fluid to the abdomen where it is absorbed. Once the shunt is in place, the ventricles usually diminish in size in 3 to 4 days, regardless of the duration of the hydrocephalus. Even though the ventricular swelling diminishes, only 21% of patients show a marked improvement in symptoms. The most likely patients to show improvement are those that show only gait disturbance, mild or no incontinence, and mild dementia. A more recent study (2004) found better outcomes, concluding that if patients with idiopathic normal pressure hydrocephalus are correctly identified, shunt insertion yielded beneficial outcomes in 86% of patients, in either gait disturbance (81%), improved continence (70%), or both. They also observed that measurements in the diagnostic clinical triad, the cortical sulci size, and periventricular lucencies were related to outcome. However, other factors such as age of the patient, symptom duration, dilation of ventricles, and the degree of presurgical dementia were unrelated to outcome.
""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.
Astasia-abasia refers to the inability to either stand or walk in a normal manner. Astasia refers to the inability to stand upright unassisted. Abasia refers to lack of motor coordination in walking. The term "abasia" literally means that the base of gait (the lateral distance between the two feet) is inconstant or unmeasurable. When seen in conversion disorder, the gait is bizarre and is not suggestive of a specific organic lesion: often the patient sways wildly and nearly falls, recovering at the last moment.
An acquired total inability to stand and walk can be seen in true neurological diseases, including stroke, Parkinson's disease, damage to the cerebellum, Guillain–Barré syndrome, normal pressure hydrocephalus and many others. In normal pressure hydrocephalus, for example, when the condition remains untreated, the patient's gait becomes shortened, with frequent shuffling and falls; eventually standing, sitting, and even rolling over in bed become impossible. This advanced state is referred to as "hydrocephalic astasia-abasia".
Astasia and/or abasia are associated with the corresponding fears of walking and/or standing, variously called stasophobia, basophobia, stasiphobia, basiphobia, stasobasophobia, stasibasiphobia, etc., sometimes turning into pathological forms, i.e. phobias.
Abasia (from Greek: "a-", without and "basis", step) is the inability to walk owing to impairment in motor coordination.
The term covers a spectrum of medical disorders such as:
- choreic abasia: caused by chorea of the legs
- paralytic abasia: caused by paralysis of the leg muscles
- spastic abasia: caused by spastic stiffening of the leg muscles
- trembling abasia: caused by trembling of the legs
Abasia is frequently accompanied by astasis, an inability to stand, see Astasia-abasia.
There are a number of different treatments that are available to treat and manage conversion syndrome. Treatments for conversion syndrome include hypnosis, psychotherapy, physical therapy, stress management, and transcranial magnetic stimulation. Treatment plans will consider duration and presentation of symptoms and may include one or multiple of the above treatments. This may include the following:
1. Explanation. This must be clear and coherent as attributing physical symptoms to a psychological cause is not accepted by many educated people in western cultures. It must emphasize the genuineness of the condition, that it is common, potentially reversible and does not mean that the sufferer is psychotic. Taking a neutral-cause-based stance by describing the symptoms as functional may be helpful, but further studies are required. Ideally, the patient should be followed up neurologically for a while to ensure that the diagnosis has been understood.
2. Physiotherapy where appropriate;
3. Occupational Therapy to maintain autonomy in activities of daily living;
4. Treatment of comorbid depression or anxiety if present.
There is little evidence-based treatment of conversion disorder. Other treatments such as cognitive behavioral therapy, hypnosis, EMDR, and psychodynamic psychotherapy, EEG brain biofeedback need further trials. Psychoanalytic treatment may possibly be helpful. However, most studies assessing the efficacy of these treatments are of poor quality and larger, better controlled studies are urgently needed. Cognitive Behavioural Therapy is the most common treatment, however boasts a mere 13% improvement rate.
There are two types of normal pressure hydrocephalus: idiopathic and secondary. The secondary type of NPH can be due to a subarachnoid hemorrhage, head trauma, tumor, infection in the central nervous system, or a complication of cranial surgery.
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.
Empirical studies have found that the prognosis for conversion disorder varies widely, with some cases resolving in weeks, and others enduring for years or decades. There is also evidence that there is no cure for Conversion Disorder, and that although patients may go into remission, they can relapse at any point. Furthermore, many patients who are 'cured' continue to have some degree of symptoms indefinitely.
Studies have shown that people with acrophobia and/or an extreme fear of falling have higher scores of SMD, or space and motion discomfort. These are physical symptoms elicited by visual or kinesthetic information that is inadequate for normal spatial orientation. Space and motion discomfort arises when conflicting information is detected among visual, kinesthetic, and vestibular sensory channels. Evidence has supported the claim that patients with anxiety and SMD rely more heavily on visual cues for postural changes.
Closely related to postural control is the sensation of vertigo: a warning signal created by a loss of postural control when the distance between the observer and visible stationary objects becomes too large, and caused by a dysfunction of the vestibular system in the inner ear. In short, it is the feeling of motion when one is actually stationary. Symptoms of vertigo include dizziness, nausea, vomiting, shortness of breath, and the inability to walk or stand. Some individuals are more reliant on visual cues to control posture than others. Vestibular sensations can arise when unsound information is detected along the sensory channels (this happens even to those with normal vestibular function), and feelings of vertigo can result in people with postural control issues.