**2.4 Clinical signs and symptoms**

Children are usually referred for wetting clothes, but not for DV. Children and parents usually do not register specific symptoms of DV, so the physician must insist on them. Typical signs are difficulty initiating micturition (hesitancy), as well as straining to overcome the resistance of the contracted urinary sphincter. The urinary stream is usually not strong because the PFMs do not relax completely, and it is often intermittent.

In an attempt to postpone voiding or suppress urgency and/or urinary incontinence, children assume characteristic positions such as crossing their legs, standing on tiptoes, squatting, or manual compression of the genitals (pelvic holding maneuvers). It is typical for girls to squat by pressing their heel against the perineum [19].

Stool retention, chronic constipation and fecal incontinence occur in more than 50% of children as a result of repeated and habitual contractions of the PFMs [9].

Plenty of data from the literature indicate an association between DV and recurrent urinary tract infections [8, 20–22]. Treatment of DV reduces recurrent urinary tract infections. About 50% of children with DV may have VUR [10].

#### **2.5 Hinman-Allen syndrome**

The most severe form of DV is Hinman-Allen syndrome, according to the authors who first described it in 1973 [5, 10]. The old term "non-neurogenic neurogenic bladder" can also be found in the literature.

This syndrome occurs in children who voluntarily and habitually contract the external urethral sphincter during uninhibited detrusor contractions, which leads to the inability of emptying the bladder. The condition is characterized by detrusor overactivity and possibly its decompensation. It is clinically manifested by daytime and nighttime wetting, urgency and overflow incontinence, chronic constipation, as well as recurrent urinary tract infections. Voiding cystourethrography reveals a trabeculated bladder, high-grade bilateral VUR and large post-void residual urine. If not treated in time, it leads to reflux nephropathy followed by kidney scarring, hypertension and progressive renal failure.
