Cutis verticis gyrata
Rare scalp condition with cerebriform ridges and furrows.
Cutis verticis gyrata (CVG) is a medical condition characterized by thickening of the scalp, resulting in ridges and furrows that give the scalp a cerebriform appearance. First reported by French dermatologist Jean-Louis-Marc Alibert in 1837, the condition was later named by German physician Paul Gerson Unna in 1907. It is considered rare, with limited research and undetermined causes, though it is not exclusively congenital.
- First reported by
- Jean-Louis-Marc Alibert (1837)
- Named by
- Paul Gerson Unna (1907)
- Field
- Dermatology
- Also known as
- Robert-Unna syndrome, bulldog scalp, corrugated skin, cutis verticis plicata, pachydermia verticis gyrata
- Classification forms
- Primary essential, primary non-essential, secondary
- Male to female ratio primary essential
- 5:1 to 6:1
Lore & Background
Cutis verticis gyrata was first documented by French dermatologist Jean-Louis-Marc Alibert in 1837. A clinical description followed in the mid-19th century, and the condition was formally named by German physician Paul Gerson Unna in 1907. The condition is identified by excessive thickening of the soft tissues of the scalp, producing visible folds, ridges, or creases that are typically soft and spongy, with the number of folds ranging from two to roughly ten. The ridges are hard and cannot be flattened on applying pressure, and the condition most often affects the central and rear regions of the scalp, though it can involve the entire scalp. Hair loss may occur over thickened areas, but hair within furrows remains normal.
Reader's Guide
Cutis verticis gyrata is significant as a rare dermatological condition with unknown causes, though it is not exclusively congenital. It is classified into primary essential, primary non-essential, and secondary forms. Primary essential CVG occurs mainly in men (male:female ratio 5:1 to 6:1), develops during or after puberty, and has no associated abnormalities. Primary non-essential CVG can be linked to neuropsychiatric disorders and ophthalmologic abnormalities. Secondary CVG arises from diseases or drugs that alter scalp structure, such as acromegaly, growth hormone use, or inflammatory processes. Diagnosis is primarily clinical, based on physical appearance, with additional tests to rule out underlying conditions. Treatment options are limited to plastic surgery, scalp reduction, subcision, dermal filler injections, and hyaluronidase injections as suggested in published journals. The condition is also a feature of several syndromes, including Beare-Stevenson cutis gyrata syndrome and hypertrophic osteoarthropathy.
Did You Know?
- The ridges in cutis verticis gyrata are hard and cannot be flattened on applying pressure.
- Primary essential CVG occurs mainly in men, with a male:female ratio of between 5:1 and 6:1.
Frequently Asked Questions
Who is Cutis verticis gyrata?
CVG is a rare dermatological condition first documented by French physician Jean-Louis-Marc Alibert in 1837, though it did not receive its current name until Paul Gerson Unna coined it in 1907. It is a scalp-specific disorder rather than a systemic one, and it is not exclusively present at birth.
What are Cutis verticis gyrata's powers/role?
Its defining trait is thickening of the scalp into deep, brain-like ridges and furrows, giving the head a cerebriform look. That folded, corrugated appearance is the sole hallmark clinicians use to identify the condition.
Why is Cutis verticis gyrata important?
Despite carrying an OMIM entry, no causative gene has ever been pinpointed, leaving its genetic architecture unresolved. It remains one of the most under-researched rare scalp disorders, with limited literature and no standardized treatment protocol.
What are Cutis verticis gyrata's aliases?
Over the years it has gone by Robert-Unna syndrome, bulldog scalp, corrugated skin, cutis verticis plicata, and pachydermia verticis gyrata. Every one of those nicknames refers to the same thickened, folded scalp presentation.
More in Genetic disorders with OMIM but no gene 1-24
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