Each year there are approximately 2 to 2.5 cases per million people with loose anagen hair syndrome. Causes
The main pathological cause of loose anagen syndrome is the absence or insufficient amount of the inner root sheath in the anagen staged hairs. This creates a gap in the linking between the inner root sheath and the hair cuticles. Both of these hair features stimulate hair growth but with this detachment in the linking, loose anagen hairs are not able to grow to a long length. The abnormalities caused by the inner root sheath creates disruption in the support and anchoring of the anagen hairs. Patients with loose anagen hair syndrome have mutations in the protein keratin K6HF, which is located in the middle of the hair shaft and inner root sheath, the companion layer. These mutations account for the phenotypical features of loose anagen syndrome. In the Huxley cells of the inner root sheath of abnormal anagen hairs, there is the formation of vacuoles and the build-up of fluid which is not usually seen. There are also dyskeratotic modifications in the Henle cells, as well as the cuticle cells in both the inner root sheath and hair shaft. The hair shaft has been reported as thin for some cases and normally structured for other loose anagen syndrome reports. The inner root sheath of normal anagen hairs usually do not have keratin in the Huxley cells, Henle cells and inner root sheath.
The olfactory nerve may also be involved in HSE, which may explain its predilection for the temporal lobes of the brain, as the olfactory nerve sends branches there. In horses, a single-nucleotide polymorphism is sufficient to allow the virus to cause neurological disease; but no similar mechanism has been found in humans. Diagnosis
Brain CT scan (with/without contrast). Complete prior to lumbar puncture to exclude significantly increased ICP, obstructive hydrocephalus, mass effectBrain MRI—Increased T2 signal intensity in frontotemporal region → viral (HSV) encephalitis

Treatment
Herpesviral encephalitis can be treated with high-dose intravenous acyclovir, which should be infused 10 mg/kg(adult) over 1 hour to avoid kidney failure. Without treatment, HSE results in rapid death in approximately 70% of cases; survivors suffer severe neurological damage. When treated, HSE is still fatal in one-third of cases, and causes serious long-term neurological damage in over half of survivors. Twenty percent of treated patients recover with minor damage. Only a small population of untreated survivors (2.5%) regain completely normal brain function. Many amnesic cases in the scientific literature have etiologies involving HSE. Earlier treatment (within 48 hours of symptom onset) improves the chances of a good recovery. Rarely, treated individuals can have relapse of infection weeks to months later. There is evidence that aberrant inflammation triggered by herpes simplex can result in granulomatous inflammation in the brain, which responds to steroids. While the herpes virus can be spread, encephalitis itself is not infectious. Other viruses can cause similar symptoms of encephalitis, though usually milder (Herpesvirus 6, varicella zoster virus, Epstein-Barr, cytomegalovirus, coxsackievirus, etc.).