The main diagnosis technique is observing the area. Then blood tests can be done to determine if there is a pre-existing condition. Family history can be considered because some of the related causes/conditions can be inherited.

Alopecia areata is usually diagnosed based on clinical features.

Trichoscopy may aid in establishing the diagnosis. In alopecia areata, trichoscopy shows regularly distributed "yellow dots" (hyperkeratotic plugs), small exclamation-mark hairs, and "black dots" (destroyed hairs in the hair follicle opening).

A biopsy is rarely needed to make the diagnosis or aid in the management of alopecia areata. Histologic findings include peribulbar lymphocytic infiltrate ("swarm of bees"). Occasionally, in inactive alopecia areata, no inflammatory infiltrates are found. Other helpful findings include pigment incontinence in the hair bulb and follicular stelae, and a shift in the anagen-to-telogen ratio towards telogen.

There is currently researching being done to find more treatments dependent on the different pre-existing conditions.

Studies are being conducted in which madarosis can be related to malignancy. A study by Groehler and Rose found that there was a statistical significance between these two. They concluded that patients malignancy lesions on the eyelid have a higher chance of having madarosis than a patient with a benign lesion. They stated that despite the fact that it is significant, the absence of madarosis does not mean the lesion cannot be malignant.

In many leprosy cases, madarosis is a symptom or a quality after diagnosis. However, in India, leprosy is common and researchers report a case of madarosis before diagnosis of leprosy with no skin lesions, only madarosis. This allowed for quicker treatment.

A main reason many people have madarosis is due to the chemotherapy drugs. There was a clinical trial in 2011 that tested an eyelash gel called bimatoprost. This gel enhanced the eyelashes in quantity and thickness. They tested this on 20 breast cancer patients who were undergoing chemotherapy. Results seemed positive, in that the group of people who used the gel had growth of eyelashes after the chemotherapy drugs.

Commonly, alopecia areata involves hair loss in one or more round spots on the scalp.

- Hair may also be lost more diffusely over the whole scalp, in which case the condition is called diffuse alopecia areata.

- Alopecia areata monolocularis describes baldness in only one spot. It may occur anywhere on the head.

- Alopecia areata multilocularis refers to multiple areas of hair loss.

- Ophiasis refers to hair loss in the shape of a wave at the circumference of the head.

- The disease may be limited only to the beard, in which case it is called alopecia areata barbae.

- If the person loses all the hair on the scalp, the disease is then called alopecia areata totalis.

- If all body hair, including pubic hair, is lost, the diagnosis then becomes alopecia areata universalis.

Alopecia areata totalis and universalis are rare.

The diagnosis of an individual with acrodermatitis enteropathica includes each of the following:

- Plasma zinc level (lab)

- Light microscopy (skin biopsy)

- Electron microscopy (histology)

Latanoprost and bimatoprost are specific PGF2a analogues applied topically, and have been found to lengthen eyelashes, darken hair pigmentation and elongate hair. Bimatoprost is available as treatment for eyelash growth. Latanoprost has shown ability to promote scalp hair density and pigmentation, and is theorized to function at the dermal papilla. A study found latanoprost ineffective on eyelashes in a patient with alopecia areata. It has also been found ineffective in treatment of eyebrow hair loss.

There is no standard treatment for alopecia universalis. Many treatments have been explored, including immunomodulatory agents such as imiquimod. Tofacitinib citrate may also have benefits. In June 2014, it was reported that a 25 year old man with almost no hair on his body grew a full head of hair, and eyebrows, eyelashes, facial, armpit and other hair, following 8 months of treatment.

Many people use unproven treatments, but there is little evidence of the effectiveness of vitamins, minerals, or other dietary supplements regrowing hair or retaining hair.

There is no cure for any congenital forms of hypertrichosis. The treatment for acquired hypertrichosis is based on attempting to address the underlying cause. Acquired forms of hypertrichosis have a variety of sources, and are usually treated by removing the factor causing hypertrichosis, e.g. a medication with undesired side-effects. All hypertrichosis, congenital or acquired, can be reduced through hair removal. Hair removal treatments are categorized into two principal subdivisions: temporary removal and permanent removal. Treatment may have adverse effects by causing scarring, dermatitis, or hypersensitivity.

Temporary hair removal may last from several hours to several weeks, depending on the method used. These procedures are purely cosmetic. Depilation methods, such as trimming, shaving, and depilatories, remove hair to the level of the skin and produce results that last several hours to several days. Epilation methods, such as plucking, electrology, waxing, sugaring, threading remove the entire hair from the root, the results lasting several days to several weeks.

Permanent hair removal uses chemicals, energy of various types, or a combination to target the cells that cause hair growth. Laser hair removal is an effective method of hair removal on hairs that have color. Laser cannot treat white hair. The laser targets the melanin color in the lower 1/3 of the hair follicle, which is the target zone. Electrolysis (electrology) uses electrical current, and/or localized heating. The U.S. Food and Drug Administration (FDA) allows only electrology to use the term "permanent hair removal" because it has been shown to be able treat all colors of hair.

Medication to reduce production of hair is currently under testing. One medicinal option suppresses testosterone by increasing the sex hormone-binding globulin. Another controls the overproduction of hair through the regulation of a luteinizing hormone.

There are several causal agents for this disorder; these can be divided into three main categories and include the following:

Sabinas brittle hair syndrome is inherited as an autosomal recessive genetic trait.

In a study by Howell et al. patients were located and studied by means of complete histories and physical examinations, analyses of serum trace metals, ceruloplasmin concentration, urine and serum amino acids, and routine metabolic urine screens. In addition, serum and urine luteinizing hormone (LH) and follicle-stimulating hormone (FSH) values were determined, and were interpreted in conjunction with total plasma estrogen, estradiol, and testosterone levels. Close examination demonstrated the scalp hairs were very brittle, coarse, wiry in texture, and broke off quite easily with mechanical trauma such as combing and brushing. Some hairs could be visualized in their follicles, which were broken off at the skin line. Most patients had accompanying hyperkeratosis (thickening of the skin) of moderate degree on exposed surfaces. Maxillary hypoplasia (midfacial retrusion) was significant in many patients. The brittle, short hair, reduced eyelashes, crowded teeth, and dull appearance created a characteristic facial appearance. Post-pubertal patients had development of secondary sexual characteristics consistent with their age, except for sparse pubic escutcheons. All cases studied demonstrated some degree of mental deficiency; I.Q.'s ranged between 50–60. A deficiency in eye–hand coordination was also noted.

Patients may be ashamed or actively attempt to disguise their symptoms. This can make diagnosis difficult as symptoms are not always immediately obvious, or have been deliberately hidden to avoid disclosure. If the patient admits to hair pulling, diagnosis is not difficult; if patients deny hair pulling, a differential diagnosis must be pursued. The differential diagnosis will include evaluation for alopecia areata, iron deficiency, hypothyroidism, tinea capitis, traction alopecia, alopecia mucinosa, thallium poisoning, and loose anagen syndrome. In trichotillomania, a hair pull test is negative.

A biopsy can be performed and may be helpful; it reveals traumatized hair follicles with perifollicular hemorrhage, fragmented hair in the dermis, empty follicles, and deformed hair shafts (trichomalacia). Multiple catagen hairs are typically seen. An alternative technique to biopsy, particularly for children, is to shave a part of the involved area and observe for regrowth of normal hairs.

Hypertrichosis is diagnosed clinically by the occurrence of hair in excess of what is expected for age, sex, and ethnicity in areas that are not androgen-sensitive. The excess can be in the form of excessive length or density and may consist of any hair type (lanugo, vellus, or terminal).

Trichomegaly is a congenital condition in which the eyelashes are abnormally long, greater than 12mm in the central area and 8mm in the peripheral. The term was first used by H. Gray in 1944 in a publication in the Stanford Medical Bulletin, though he was only the third person to characterize the disorder; the first two reports were published in German in 1926 and 1931 by Reiter and Bab, respectively. Gray suggested the use of the term "movie lashes" to describe this condition, for long lashes were at the time being portrayed in film as a desirable characteristic in women.

Acrodermatitis enteropathica without treatment is fatal, and affected individuals may die within a few years. There is no cure for the condition. Treatment includes lifelong dietary zinc supplementation.

When it occurs in early childhood (before five years of age), the condition is typically self-limiting and intervention is not required. In adults, the onset of trichotillomania may be secondary to underlying psychiatric disturbances, and symptoms are generally more long-term.

Secondary infections may occur due to picking and scratching, but other complications are rare. Individuals with trichotillomania often find that support groups are helpful in living with and overcoming the disorder.

Alopecia universalis can occur at any age, and is currently believed to be an autoimmune disorder, in which a person's immune system attacks the hair follicles. Genetic factors may contribute to AU as approximately 20% of those affected have a family member with alopecia.

Diagnosis of mitochondrial trifunctional protein deficiency is often confirmed using tandem mass spectrometry. It should be noted that genetic counseling is available for this condition. Additionally the following exams are available:

- CBC

- Urine test

Seborrhea is recognized as an androgen-sensitive condition – that is, it is caused or aggravated by androgen sex hormones such as testosterone and dihydrotestosterone – and is a common symptom of hyperandrogenism (e.g., that seen in polycystic ovary syndrome). In addition, seborrhea, as well as acne, are commonly associated with puberty due to the steep increase of androgen levels at that time.

In accordance with the involvement of androgens in seborrhea, antiandrogens, such as cyproterone acetate, spironolactone, and flutamide, are highly effective in alleviating the condition. As such, they are used in the treatment of seborrhea, particularly severe cases. While beneficial in seborrhea, effectiveness may vary with different antiandrogens; for instance, spironolactone (which is regarded as a relatively weak antiandrogen) has been found to produce a 50% improvement after three months of treatment, whereas flutamide has been found to result in an 80% improvement within three months. Cyproterone acetate is similarly more potent and effective than spironolactone, and results in considerable improvement or disappearance of acne and seborrhea in 90% of patients within three months.

Systemic antiandrogen therapy should only be used to treat seborrhea in women, as these drugs can result in feminization (e.g., gynecomastia), sexual dysfunction, and infertility in males. In addition, antiandrogens theoretically have the potential to feminize male fetuses in pregnant women, and for this reason, should always be combined with effective contraception in sexually active women who can or may become pregnant.

Poliosis, also called poliosis circumscripta, is the decrease or absence of melanin (or colour) in head hair, eyebrows, eyelashes or any other hairy area. It is popularly known as white forelock when it affects hair right above the forehead.

This condition can cause single or, less commonly, multiple white patches on the hair. Some mistake these white patches for simple birth marks. In poliosis there is decreased or absent melanin in the hair bulbs of affected hair follicles; the melanocytes of the skin are usually not affected. Poliosis occurs in several genetic syndromes such as piebaldism, Waardenburg syndrome, neurofibromatosis type I, and tuberous sclerosis. It can also occur in conditions such as vitiligo, Vogt–Koyanagi–Harada disease, alopecia areata, sarcoidosis, and in association with neoplasms and some medications.

It can give rise to a "Mallen streak" that can be hereditary. Catherine Cookson wrote a novel and later a TV series called "The Mallen Streak", where a family had the condition. Sports presenter Dickie Davies, runner Sam Brown, and fashion expert Stacy London were famous for their respective Mallen streak.

Daily use of an over-the-counter or prescription anti-fungal shampoo containing ketoconazole or zinc pyrithione may help in those with recurrent episodes of the disease.

Both natural and artificial UV radiation curbs the growth of "Malassezia" yeast.

TS can be diagnosed based on clinical observations, but is usually confirmed by histopathology of a lesional biopsy or a plucked spicule. Characteristic histological findings include enlarged and abnormally organized hair follicles and hyperproliferation of inner root sheath cells containing large eosinophilic trichohyalin granules. Antibodies against major capsid protein VP1, the major component of the viral capsid, can be used to confirm the presence of viral particles in cell nuclei. Electron microscopy can also be used to detect viral particles. Quantification of viral load can be performed using quantitative PCR, as affected skin demonstrates much higher viral loads compared to unaffected skin or to asymptomatic individuals who test positive for viral DNA.

Differential diagnosis includes other visually similar conditions affecting the hair follicles, many of which appear as drug side effects. A proposed classification system lists TS as one of a group of cutaneous conditions with similar manifestations and distinct etiologies, collectively called the digitate keratoses. Although confirmed TS is very rare, the condition is thought to be underdiagnosed.

Symptoms include brittle hair, mild mental retardation and nail dysplasia. The syndrome was first observed in Sabinas, a small community in northern Mexico.

The principal biochemical features of the illness are reduced hair cystine levels, increased copper/zinc ratio, and presence of arginosuccinic acid in the blood and urine.

The key finding is brittle hair with low sulfur content, but alternating dark and light bands under polarizing microscopy, trichoschisis, and absent or defective cuticle are additional important clues for the diagnosis of trichothiodystrophy. Review of literature reveals extensive associated findings in trichothiodystrophy. Amino acid analyses of control hair when compared with those of patients with the Sabinas syndrome showed very striking differences with regard to content of sulphur amino acids. As in previous descriptions of amino acid abnormalities in the trichorrhexis nodosa of arginosuccinicaciduria, there were increases in lysine, aspartic acid, alanine, leucine, isoleucine, and tyrosine.

Trichothiodystrophy represents a central pathologic feature of a specific hair dysplasia associated with several disorders in organs derived from ectoderm and neuroectoderm. Trichothiodystrophy or TTD is a heterogeneous group of autosomal recessive disorders, characterized by abnormally sulfur deficient brittle hair and accompanied by ichthyosis and other manifestations.

Patients with trichothiodystrophy should have a thorough evaluation for other associated manifestations, including investigation of photosensitivity and DNA repair defects. Because the disease appears to be inherited in an autosomal recessive pattern, detection of low-sulfur brittle hair syndrome is also important for genetic counseling.

Screening generally only takes place among those displaying several of the symptoms of ABCD, but a study on a large group of institutionalized deaf people in Columbia revealed that 5.38% of them were Waardenburg patients. Because of its rarity, none of the patients were diagnosed with ABCD (Waardenburg Type IV). Nothing can be done to prevent the disease.

For demodectic mange, properly performed deep skin scrapings generally allow the veterinarian to identify the microscopic mites. Acetate tape impression with squeezing has recently found to be a more sensitive method to identify mites. It was originally thought that because the mite is a normal inhabitant of the dog's skin, the presence of the mites does not conclusively mean the dog suffers from demodex. Recent research, however, found that demodex mite can hardly be found on clinically normal dogs, meaning that the presence of any number of mites in a sample is very likely to be significant. In breeds such as the West Highland White Terrier, relatively minor skin irritation which would otherwise be considered allergy should be carefully scraped because of the predilection of these dogs to demodectic mange. Skin scrapings may be used to follow the progress of treatment in demodectic mange.

Alternatively, plasma levels of zinc and copper have been seen to be decreased in dogs suffering with demodicosis. This may be due to inflammation involved in the immune response of demodicosis which can lead to oxidative stress resulting in dogs suffering from demodicosis to exhibit higher levels of antioxidant productivity. The catalases involved in the antioxidant pathway require the trace minerals zinc and copper. Dogs with demodicosis show a decrease in plasma copper and zinc levels due to the increased demand for antioxidant activity. Therefore, this may be considered as a potential marker for demodicosis.