Treatment of Ramsay Hunt Syndrome Type 1 is specific to individual symptoms. Myoclonus and seizures may be treated with drugs like valproate.

Some have described this condition as difficult to characterize.

RHS type 1 is caused by the impairment of a regulatory mechanism between cerebellar and brainstem nuclei and has been associated with a wide range of diseases, including Lafora disease, dentatorubropallidoluysian atrophy, and celiac disease.

There are many causes of cerebellar ataxia including, among others, gluten ataxia, autoimmunity to Purkinje cells or other neural cells in the cerebellum, CNS vasculitis, multiple sclerosis, infection, bleeding, infarction, tumors, direct injury, toxins (e.g., alcohol), genetic disorders, and an association with statin use. Gluten ataxia accounts for 40% of all sporadic idiopathic ataxias and 15% of all ataxias.

Cerebellar ataxia is a form of ataxia originating in the cerebellum. Non-progressive congenital ataxia (NPCA) is a classical presentation of cerebral ataxias.

Intention tremors are common among individuals with multiple sclerosis (MS). One common symptom of multiple sclerosis is ataxia, a lack of coordinated muscle movement caused by cerebellar lesions characteristic of multiple sclerosis. The disease often destroys physical and cognitive function of individuals.

Intention tremors can be a first sign of multiple sclerosis, since loss or deterioration of motor function and sensitivity are often one of the first symptoms of cerebellar lesions.

Intention tremors have a variety of other recorded causes as well. These include a variety of neurological disorders, such as stroke, alcoholism, alcohol withdrawal, peripheral neuropathy, Wilson's disease, Creutzfeldt–Jakob disease, Guillain–Barré syndrome and fragile X syndrome, as well as brain tumors, low blood sugar, hyperthyroidism, hypoparathyroidism, insulinoma, normal aging, and traumatic brain injury. Holmes tremor, a rubral or midbrain tremor, is another form of tremor that includes intention tremors, among other symptoms. This disease affects the proximal muscles of the head, shoulders, and neck. Tremors of this disease occur at frequencies of 2–4 Hz or more.

Intention tremor is also known to be associated with infections, West Nile virus, rubella, H. influenza, rabies, and varicella. A variety of poisons have been shown to cause intention tremor, including mercury, methyl bromide, and phosphine. In addition, vitamin deficiencies have been linked to intention tremor, especially deficiency in vitamin E. Pharmacological agents such as anti-arrhythmic drugs, anti-epileptic agents, benzodiazepine, cyclosporine, lithium, neuroleptics, and stimulants have been known to cause intention tremor. Some ordinary activities including ingesting too much caffeine, cigarettes, and alcohol, along with stress, anxiety, fear, anger and fatigue

have also been shown to cause intention tremor by negatively affecting the cerebellum, brainstem, or thalamus, as discussed in mechanisms.

Botulinum A toxin is a valuable alternative for patients who do not want surgical methods.

Intention tremor, also known as cerebellar tremor, is a dyskinetic disorder characterized by a broad, coarse, and low frequency (below 5 Hz) tremor. The amplitude of an intention tremor increases as an extremity approaches the endpoint of deliberate and visually guided movement (hence the name intention tremor). An intention tremor is usually perpendicular to the direction of movement. When experiencing an intention tremor, one often overshoots or undershoots their target, a condition known as dysmetria. Intention tremor is the result of dysfunction of the cerebellum, particularly on the same side as the tremor in the lateral zone, which controls visually guided movements. Depending on the location of cerebellar damage, these tremors can be either unilateral or bilateral.

A variety of causes have been discovered to date, including damage or degradation of the cerebellum due to neurodegenerative diseases, trauma, tumor, stroke, or toxicity. There is currently no established pharmacological treatment; however, some success has been seen using treatments designed for essential tremors.

The pathophysiology of the condition results from neuronal plasticity associated with bladder afferents and motor neurons innervating the external urethral sphincter. People with this condition generally experience daytime and night time wetting, urinary retention, and often have a history of urinary tract and bladder infections. Constipation and encopresis are often associated with this condition.

Several definitions have been offered:

- "Absence of normal relaxation of pelvic floor muscles during defecation, resulting in rectal outlet obstruction".

- "Malfunction (a focal dystonia) of the external anal sphincter and puborectalis muscle during defecation".

- "[...] failure of [the external anal sphincter and puborectalis] muscle[s] to relax, resulting in maintenance of the anorectal angle and the difficulty with initiating and completing bowel movements".

- "[...] failure of relaxation (or paradoxic contraction) of the puborectalis muscle sling during defaecation, attempted defaecation or straining."

Anismus is classified as a functional defecation disorder. It is also a type of rectal outlet obstruction (a functional outlet obstruction). Where anismus causes constipation, it is an example of functional constipation. Some authors describe an "obstructed defecation syndrome", of which anismus is a cause.

The Rome classification subdivides functional defecation disorders into 3 types, however the symptoms the patient experiences are identical.

- Type I: paradoxical contraction of the pelvic floor muscles during attempted defecation

- Type II: inadequate propulsive forces during attempted defecation (inadequate defecatory propulsion)

- Type III: impaired relaxation with adequate propulsion

It can be seen from the above classification that many of the terms that have been used interchangeably with anismus are inappropriately specific and neglect the concept of impaired propulsion. Similarly, some of the definitions that have been offered are also too restrictive.

There are two types of prostatic stent: temporary and permanent.

Although a permanent prostatic stent is not a medical treatment, it falls under the classification of a surgical procedure. Placement of a permanent prostatic stent is carried out as an outpatient treatment under local, topical or spinal anesthesia and usually takes about 15–30 minutes.

A temporary prostatic stent can be inserted in a similar manner to a Foley catheter, requiring only topical anesthesia.

A prostatic stent is a stent used to keep open the male urethra and allow the passing of urine in cases of prostatic obstruction and lower urinary tract symptoms (LUTS). Prostatic obstruction is a common condition with a variety of causes. Benign prostatic hyperplasia (BPH) is the most common cause, but obstruction may also occur acutely after treatment for BPH such as transurethral needle ablation of the prostate (TUNA), transurethral resection of the prostate (TURP), transurethral microwave thermotherapy (TUMT), prostate cancer or after radiation therapy.

The prognosis for non-ischemic cases of SBO is good with mortality rates of 3–5%, while prognosis for SBO with ischemia is fair with mortality rates as high as 30%.

Cases of SBO related to cancer are more complicated and require additional intervention to address the malignancy, recurrence, and metastasis, and thus are associated with poorer prognosis.

All cases of abdominal surgical intervention are associated with increased risk of future small-bowel obstructions. Statistics from U.S. healthcare report 18.1% re-admittance rate within 30 days for patients who undergo SBO surgery. More than 90% of patients also form adhesions after major abdominal surgery.

Common consequences of these adhesions include small-bowel obstruction, chronic abdominal pain, pelvic pain, and infertility.

Fetal and neonatal bowel obstructions are often caused by an intestinal atresia, where there is a narrowing or absence of a part of the intestine. These atresias are often discovered before birth via an ultrasound, and treated with using laparotomy after birth. If the area affected is small, then the surgeon may be able to remove the damaged portion and join the intestine back together. In instances where the narrowing is longer, or the area is damaged and cannot be used for a period of time, a temporary stoma may be placed.