A cross-sectional examination of a loose anagen hair displays irregularity such as the shape of the hair being triangular rather than oval. The electron microscopy scanned image of the inner root sheath of a loose anagen hair would exhibit ultrastructural changes. These changes are visible in the Huxley layer, Henle layer and the cuticle of the loose anagen hair. An electron microscopy image of outer root sheath of an loose anagen hair would display malformations and weak linkage in the cells within the epithelium of the outer root sheath. This irregularity within the outer root sheath of a loose anagen hair is considered the most notable change when examining a loose anagen hair under an electron microscope.In a histopathological examination, the different layers of the loose anagen hair follicle will display a deficiency of clarity between the layers. This incoherence is also visible in a histological slide of the inner root sheath and of the outer root sheath.Biopsies are not necessary for the diagnosis of loose anagen hair syndrome. A biopsy will display non-inflammatory, non-scarring alopecia.The texture of the hair varies with some reports stating that patients with loose anagen syndrome have hairs that are rough, brittle and sticky. This may be the result of the deformations of the hair shaft. These changes in texture limits the ability for adjacent loose anagen hairs to rest flat on the scalp. The patient can have thinning and loss of hair around the whole scalp, at the occipital scalp or around the scalp in odd, irregular patches.
Idiopathic pure sudomotor failure (IPSF) is the most common cause of a rare disorder known as acquired idiopathic generalized anhidrosis (AIGA), a clinical syndrome characterized by generalized decrease or absence of sweating without other autonomic and somatic nervous dysfunctions and without persistent organic cutaneous lesions.The term IPSF was first introduced in 1994 after researchers at Saitama Medical School speculated the primary lesion sites in patients were within cholinergic receptors of the sweat glands. The term IPSF represent a distinct subgroup of AIGA without sudomotor neuropathy or sweat gland failure. Clinical features
Early onset in life
Acute or sudden onset
Concomitant sharp pain or cholinergic urticaria over the entire body
Absence of other autonomic dysfunction
Elevated serum IgE levels
Marked response to glucocorticoids
Preserved apocrine sweating (adrenergic innervation)

Pathology
Intracutaneous injection of pilocarpine (sweat gland stimulant) is known to evoke no sweat response, indicating that lesions are on the post-synaptic side of the nerve-sweat gland junction.The proposed pathomechanisms of idiopathic pure sudomotor failure include:

A deficit within muscarinic cholinergic receptors of the eccrine sweat glands. Interference in acetylcholine transmission to cholinergic receptors. A cross-reactive immune response which interferes with cholinergic transmission in the eccrine glands. Components of an immediate-type allergy (based on the dramatic resumption of axon reflex sweating following glucocorticoid treatment). Diagnosis
Management
Treatment of AIGA almost always consists of steroid pulse therapy or high-dose oral steroids and is not consistently effective. Much remains unclear regarding the reasons for recurrent anhidrosis.