Bernard Nusbaum, M.D.
Miami, Florida
With increasing consumer awareness regarding hair transplantation, patients with alopecias of different etiologies will present to the hair transplant surgeon rather than to dermatologists or general practitioners. Some of these conditions, if transplanted, can result in failure. A guide for recognition and management of these patients is presented.
These patients make up the majority of patients who are candidates for hair transplantation, as long as no other contraindications exist. The key to their recognition is to begin the scalp examination by looking for patterns.
Androgenetic alopecia will generally fit into a Norwood or Ludwig type of pattern. Post surgical alopecia (most commonly seen after some face-lift procedures) is evident by history and typical areas of alopecia in the temporal-preauricular-nape areas or in coronal scars. Traction alopecia usually occurs in the temporal and frontal areas although the occipital area can also be affected. In traction alopecia terminal hair growth is evident at the periphery of the affected area and sparse vellus hairs are present at the center of the involved areas (Fig. 1).
If one does not recognize these patterns, an index of suspicion should immediately arise that we need to look further and perform a more thorough history and physical examination. With regard to the scalp examination it is important to determine whether the alopecia is SCARRING vs. NON-SCARRING. A cursory way to make this determination is to recognize that in a scarring alopeica the skin is smooth, and devoid of pores. Scarring alopeicas will be discussed later in this article but it should be mentioned that when you see scarring alopecia, the next thought should be to perform a scalp biopsy, since this will be necessary for diagnostic confirmation.
Another aspect of the scalp examination is what is termed the Hair Pull Test, a very important tool in the evaluation of diffuse alopecia. The hair pull test involves gently pulling 50-100 hairs between the thumb and forefinger proximally to distally. If no more than five telogen hairs are obtained the test is considered normal. The hair pull test is increased 3x-4x in a condition termed Telogen Effluvium which will be discussed next.
Telogen effluvium is second only to androgenetic alopecia as a cause of hair loss in women. Patients with this condition generally give a history of increased hair shedding rather than just thinning. The history should focus on identifying a precipitating event 3 months prior to the onset such as childbirth, high fever, general anesthesia, sudden weight loss, diets deficient in protein or a hormonal change. It can also be drug-induced (Table 1) or associated with systemic disease.
Hair thinning in these patients is non-scarring, diffuse and not patterned, although it is frequently most obvious in the temporal areas. In telogen effluvium the hair pull test is abnormal all over the scalp and to a greater degree than in androgenetic alopecia where the hair pull test may be abnormal in affected areas but normal in the occiput. If there is a doubt in the diagnosis, a scalp biopsy will differentiate these 2 entities. It should be noted that patients with androgenetic alopecia can have concomitant telogen effluvium and in that case a biopsy will show features of both conditions.
When a woman presents with diffuse alopecia of undetermined origin, work-up should include a thyroid profile, RPR, serum iron and ferritin, and an ANA. If there are signs of virilization or polycystic ovarian disease, DHEAS/testosterone and prolactin levels should be ordered respectively. If any of these tests are abnormal it is advisable to defer transplantation until the underlying problem has been corrected, time has been allowed for any spontaneous hair regrowth to occur and a definitive diagnosis can be made. If one is certain that the underlying diagnosis is androgenetic alopecia and the patient is a good candidate, then one can proceed with transplantation. Hair transplantation is not indicated in telogen effluvium and the mainstay of treatment is reassurance, since generally the problem resolves spontaneously in 3-6 months. Some cases can go on for several years and these patients are categorized as having chronic telogen effluvium.
This is the most common alopecia seen in a dermatology office. In its most common form, it presents as a patchy, non-scarring alopecia (Fig. 2) that can involve the head, eyebrows and any other hair bearing areas. Clues to diagnosis include recognition of "exclamation-point hairs" which are fractured hairs, 3-4 mm in length with the distal end broader in diameter than the proximal segment. Also, when regrowth occurs (spontaneously or with medical treatment), it begins initially with growth of depigmented, white hairs.
In its classical form, alopecia areata is relatively easy to recognize. Of utmost importance to the hair restoration surgeon however, is to beware that this condition can present as diffuse alopecia areata (Fig. 3). In this less common form it may be clinically indistinguishable from androgenetic alopecia and the only way to confirm the diagnosis is by scalp biopsy.
Alopecia areata is an autoimmune, inflammatory process that can attack any hair follicle and result in lack of growth or subsequent loss of transplanted hairs.
Triangular alopecia is characterized by a lancet or oval shaped non-scarring hairless patch in the frontotemporal region of the scalp with the apex usually pointing to the vertex (Fig. 4). Usually some vellus hair are visible within the patch. The condition is present at birth and has been reported to occur in 0.11% of the general population3 but is probably more common than the small number of reported cases might suggest4. The characteristic shape and the fact that the patch has not undergone change help to differentiate this entity from alopecia areata. Histology confirms the clinical findings of presence of vellus hairs and absence of terminal hairs5.
Dr. Richard Shiell6 has grafted five patients with this condition and has performed scalp reduction on two patients with good results (Shiell R. personal communication).
The author has recently transplanted two patients with triangular alopecia utilizing follicular units and results are pending.
This entity is an impulse-control disorder which can affect single or multiple areas of varying size. Physical examination reveals twisted and broken hair shafts of various lengths. This incomplete nature of the hair loss is a "tip-off" to its diagnosis and trichotillomonia has a distinctive histopathology.
These patients should not be transplanted and referral to a psychologist or psychiatrist is indicated.
Included in this group are Lichen planopilaris, Fibrosing Alopecia in a Pattern Distribution1, Pseudopelade, Morphea, Discoid Lupus and Folliculitis Decalvans. Each of these entitities has distinctive histopathologic features and have been reviewed2.
The typical clinical appearance consists of areas a few millimeters in diameter which can coalesce to form larger patches in which hair loss occurs and the skin appears white, shiny and without follicular orifices (Fig. 5). In areas where there is active disease (which typically are at the periphery of the alopecic areas) there is evidence of inflammation with perifollicular erythema and scaling.
When scarring alopecia is suspected, a skin biopsy is mandatory. It will not only confirm the diagnosis but will determine disease activity. The biopsy specimen should be 4-6 mm in diameter, should include the subcutaneous fat and be obtained from the edge of the alopecic area. The specimen should be sent to an experienced dermatopathologist.
The management of cicatrical alopecia entails monitoring these patients after successful medical treatment to assure that there is no disease activity for 12 months prior to surgical intervention. It would be wise to perform test grafts initially to document viable growth prior to embarking on a regular transplant session. Since there may be compromised circulation in the alopecic area, use fewer grafts and place them further apart with longer intervals between sessions. Finally consider alopecia reduction as an adjunct to the overall surgical plan.
A new subset of scarring alopecia that follows the distribution of androgenetic alopecia has been described recently1,7. It is interesting that the immune system of these patients recognizes miniaturizing follicles as being abnormal consequently targetting them with inflammation and subsequent destruction. I am currently treating one of these patients (Fig. 6) with the hope that disease activity will subside and I can attempt transplantation.
In summary, if one performs enough hair transplant consultations, you will see some of these patients; and when you do, you should be able to recognize them and either manage the case or refer them to the appropriate specialist. As hair transplant surgery continues to become more of an interdisciplinary specialty we must assure that proper training in scalp disorders is provided.
Table I
| Common Drugs That Can Cause Telogen Effluvium |
| Oral Contraceptives |
| Androgens |
| Cimetidine |
| Beta Blockers |
| Coumadin, Heparin |
| Anticholesterol Agents |
| Vitamin A |
| ACE inhibitors |
| Lithium |
Fig 1: Typical traction alopecia pattern.
Fig 2: Classical Alopecia Areata
Fig 3: Diffuse Alopecia Areata: Note similarity to female pattern alopecia.
Fig 4: Triangular Alopecia. Unlike Alopecia Areata this entity is present at birth and is unchanging.
Fig 5: Typical appearance of end-stage scarring alopecia
Fig 6: Fibrosing Alopecia in a Pattern Distribution. Biopsy showed changes consistent with Lichen Planopilaris.
- Zingernagel MS, Trueb RM. Fibrosing Alopecia in a pattern distribution: patterned lichen planopilaris or androgenetic alopecia with a lichenoid tissue reaction pattern? Arch Dermatol. 2000;135:205-211.
- Sperling LC. A New Look at Scarring Alopecia. Arch Dermatol. 2000;136:235-232.
- Garcia-Hernandez MJ, Rodriguez-Pichardo A, Camacho F. Congential triangular alopecia (Beauer Nevus). Pediatr. Dermatol. 1995;12:301-303.
- Tosti A. Congenital triangular alopecia. J. Am. Acad. Dermatol. 1987;16:991-993.
- Minars N. Congenital temporal alopecia. Arch. Dermatol. 1974;109:395-396.
- Shiell R. Hair Transplant Forum International Vol. 9 No 6. p.192.
- Avram MR. Hair Transplant Forum International. May/June 2000.