Trigonocephaly is a congenital condition of premature fusion of the metopic suture (from the Greek metopon, "forehead"), leading to a triangular forehead. The merging of the two frontal bones leads to transverse growth restriction and parallel growth expansion. It may occur syndromic, involving other abnormalities, or isolated. The term is from the Greek trigonon, "triangle", and kephale, "head". Cause
Trigonocephaly can either occur syndromatic or isolated. Trigonocephaly is associated with the following syndromes: Opitz syndrome, Muenke syndrome, Jacobsen syndrome, Baller–Gerold syndrome and Say–Meyer syndrome. The etiology of trigonocephaly is mostly unknown although there are three main theories. Trigonocephaly is probably a multifactorial congenital condition, but due to limited proof of these theories this cannot safely be concluded. Intrinsic bone malformation
The first theory assumes that the origin of pathological synostosis lies within disturbed bone formation early on in the pregnancy. Causes can either be genetic (9p22–24, 11q23, 22q11, FGFR1 mutation), metabolic (TSH suppletion in hypothyroidism) or pharmaceutical (valproate in epilepsy). Fetal-head constraint
The second theory says that synostosis begins when the fetal head gets hindered in the pelvic outlet during birth. Intrinsic brain malformation
The third theory predominates disturbed brain formation of the two frontal lobes as the main issue behind synostosis. Limited growth of the frontal lobes leads to an absence of stimuli for cranial growth, therefore causing premature fusion of the metopic suture.
Such symptoms include:
Increased thirst
Increased urination, especially waking up in the night to urinate
Tiredness and fatigue
Blurred vision
Slow healing of wounds
Altered sensation, such as numbness or tingling, particularly of the hands and feet
Recurrent, and difficult to clear infections, particularly of the urinary tract

Risk factors
As impaired fasting glucose is considered a precursor condition for type 2 diabetes, it shares the same environmental and genetic risk factors. Diagnosis
Different organisations use slightly differing levels before classifying a persons fasting blood glucose as "impaired", with the American Diabetes Association using a lower cutoff in its criteria than the World Health Organization. The upper limits remain the same, as fasting levels above this are almost universally accepted as indicative of full diabetes:

WHO criteria: fasting plasma glucose level from 6.1 mmol/L (110 mg/dL) to 6.9 mmol/L (125 mg/dL). ADA criteria: fasting plasma glucose level from 5.6 mmol/L (100 mg/dL) to 6.9 mmol/L (125 mg/dL). Prevention
The guidelines for preventing impaired fasting glucose are the same as those given for preventing type 2 diabetes in general. If these are adhered to, the progression to clinical diabetes can be slowed or halted. In some cases, a complete reversal of IFG can be achieved. Certain risk factors, such as being of Afro-Caribbean or South Asian ethnicity, as well as increasing age, are unavoidable, and such individuals may be advised to follow these guidelines, as well as monitor their blood glucose levels, more closely. Management
References


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