Other problems that can contribute to anal itching include pinworms, hemorrhoids, tears of the anal skin near the mucocutaneous junction (fissures), and skin tags (abnormal local growth of anal skin). Aside from diseases relative to the condition, a common view suggests that the initial cause of the itch may have passed, and that the illness is in fact prolonged by what is known as an itch-scratch-itch cycle. It states that scratching the itch encourages the release of inflammatory chemicals, which worsen redness, intensifies itchiness and increases the area covered by dry skin, thereby causing a snowball effect. Some authorities describe “psychogenic pruritus” or "functional itch disorder", where psychological factors may contribute to awareness of itching. Ingestion of pinworm eggs leads to enterobiasis, indicative of severe itching around the anus from migration of gravid females from the bowel. Severe cases of enterobiasis result in hemorrhage and eczema. Diagnosis
Diagnosis is usually done with a careful examination of the anus and the patients history. If the presentation or physical findings are atypical, biopsies can be done.In case of long-lasting symptoms, above all in patients over 50 years of age, a colonoscopy is useful to rule out a colonic polyp or tumor, that can show pruritus ani as first symptom. Treatment
The goal of treatment is asymptomatic, intact, dry, clean perianal skin with reversal of morphological changes. For pruritus ani of unknown cause (idiopathic pruritus ani) treatment typically begins with measures to reduce irritation and trauma to the perianal area. Stool softeners can help prevent constipation.
Frontotemporal dementia (Picks disease)
Gerstmann–Sträussler–Scheinker syndrome
Huntingtons disease
Lytico-bodig disease (ALS complex of Guam)
Multiple system atrophy (Shy–Drager syndrome)
Neuroacanthocytosis
Neuronal ceroid lipofuscinosis
Olivopontocerebellar atrophy
Pantothenate kinase-associated neurodegeneration, also known as neurodegeneration with brain iron accumulation
Parkin mutation (hereditary juvenile dystonia)
Parkinsons disease
Parkinsons disease dementia
Progressive supranuclear palsy
Wilsons disease
X-linked dystonia parkinsonism (Lubag syndrome)

Drug-induced ("pseudoparkinsonism")
About 7% of people with parkinsonism developed symptoms as a result of side effects of medications, mainly neuroleptic antipsychotics especially the phenothiazines (such as perphenazine and chlorpromazine), thioxanthenes (such as flupenthixol and zuclopenthixol) and butyrophenones (such as haloperidol), and rarely, antidepressants. Yet another drug that can induce parkinsonism is the antihistaminic medication cinnarizine, usually prescribed for motion sickness; this is because besides antagonizing histamine receptors this drug antagonizes the dopamine D2 receptors. The incidence of drug-induced parkinsonism increases with age. Drug-induced parkinsonism tends to remain at its presenting level and does not worsen like Parkinsons disease.Implicated medications include:

Antipsychotics
Lithium
Metoclopramide
MDMA addiction and frequent use
Tetrabenazine
Cinnarizine

Infectious
Creutzfeldt–Jakob disease
Encephalitis lethargica
HIV infection and AIDS

Toxins
Evidence exists of a link between exposure to pesticides and herbicides and PD; a two-fold increase in risk was seen with paraquat or maneb/mancozeb exposure.Chronic manganese (Mn) exposure has been shown to produce a parkinsonism-like illness characterized by movement abnormalities. This condition is not responsive to typical therapies used in the treatment of PD, suggesting an alternative pathway than the typical dopaminergic loss within the substantia nigra. Manganese may accumulate in the basal ganglia, leading to the abnormal movements. A mutation of the SLC30A10 gene, a manganese efflux transporter necessary for decreasing intracellular Mn, has been linked with the development of this parkinsonism-like disease.