Type 2: Spiny keratoderma (also known as "Porokeratosis punctata palmaris et plantaris," "Punctate keratoderma," and "Punctate porokeratosis of the palms and soles") is an autosomal dominant keratoderma of late onset that develops in patients aged 12 to 50, characterized by multiple tiny keratotic plugs, resembling the spines on a music box, involving the entire palmoplantar surfaces. : 509 
Type 3: Focal acral hyperkeratosis (also known as "Acrokeratoelastoidosis lichenoides," and "Degenerative collagenous plaques of the hand") is a late-onset keratoderma, inherited as an autosomal dominant condition, characterized by oval or polygonal crateriform papules developing along the border of the hands, feet, and wrists. : 509  It is considered similar to Costa acrokeratoelastoidosis. Ungrouped
Palmoplantar keratoderma and spastic paraplegia (also known as "Charcot–Marie–Tooth disease with palmoplantar keratoderma and nail dystrophy") is an autosomal dominant or x-linked dominant condition that begins in early childhood with thick focal keratoderma over the soles and, to a lesser extent, the palms. : 513 
Palmoplantar keratoderma of Sybert (also known as "Greither palmoplantar keratoderma," "Greither syndrome," "Keratosis extremitatum hereditaria progrediens," "Keratosis palmoplantaris transgrediens et progrediens" "Sybert keratoderma," and "Transgrediens and progrediens palmoplantar keratoderma") is an extremely rare autosomal dominant keratoderma (a skin condition involving horn-like growths) with symmetric severe involvement of the whole palmoplantar surface in a glove-and-stocking distribution. : 509  It was characterized by Aloys Greither in 1952. It was characterized by Virginia Sybert in 1988. An autosomal recessive form which is known as Mal de Meleda has been described. This is associated with mutations in the Secreted Ly-6/uPAR-related protein 1 (SLURP1) gene.
Traction alopecia: history of tight hairstyles and marginal hairline
Trichotillomania: history of pulling hair or evidence of traumatic folliclesPull Test
This test is performed to estimate the severity of hair loss and refine the differential diagnosis. A clinician grabs sections of hair and observes for active hair loss. A positive pull test is usually caused by telogen effluvium, androgenetic alopecia, and alopecia areata.Tug Test
A doctor holds the top and bottom of a strand of hair and observes for a break in the middle which may be caused by a hair shaft abnormality.Card Test
A part in the hair is created and a small card is placed to contrast the color of the hair and visualize thin strands of hair (seen in telogen effluvium) vs short broken strands (seen in hair shaft abnormalities).Fungal Culture
Scalp is scraped and the specimen is incubated for fungal growth commonly seen in tinea capitis.Scalp biopsy
If the diagnosis of hair loss is unclear or not responsive to the treatment, a scalp biopsy may be required. Scalp biopsy will show evidence of inflammation, location, and change in the follicles. This will frequently refine the diagnosis.Blood Tests
In the case of suspected iron deficiency, thyroid disease, or androgen excess a blood test may be necessary to rule in these causes.Trichoscopy
A new technique which allows for magnified visualization of the hair and scalp, providing a high definition, detailed look at follicles. Treatment
Steroids
Steroids may be used for the short-term treatment of autoimmune causes of hair loss such as alopecia areata.