HYPOTHESIS

PRIMARY ENURESIS: A NEURODEVELOPMENTAL DISORDER

N.R. ARUNKISHORE

Department of psychiatry,

Medical College Hospital, Trichur
      Enuresis has puzzled physicians for centuries. Theories regarding the etiology of the disorder have ranged from the psycho-analytical to behavioural to pure physical, changing with the current scientific thinking if the times.
      It is well known that most enuretics recover from their disorder, often without treatment, as they grow up. The prevalence of enuresis in children has been estimated to be 52.2/1000 (Verghese & Beig, 1974). Shalini kurup in her community based study found it to be the commonest psychiatric problem affecting children (prevalence of 9.2%). Though the exact prevalence of enuresis in adults is difficult to be determined, Forsythe and Redmond (1974) found that 3% of 1129 enuretics were still wetting after the age of 20 years. Thus most children appear to have a developmental lag in attaining bladder control.
      The high prevalence rates of enuresis on children raises certain questions. The high spontaneous cure rate may mean a developmental delay (maturational slowing)
      Enuresis commonly runs in families. There is a definitly higher rate of enuresis in first degree relatives of enuretic children. Shaeffer et al (1984) found 85% of children gave a family history of enuresis. 70% of children studied had a positive family history of enuresis compared to the control group (Kishore, 1988).
      Bakwin (1971) in an exhaustive study of 338 twins found that if a parent had been enuretic in childhood, 40% of the children were wetters. When neither parent gave a history of enuresis in childhood the incidence of enuresis in their children was 15%. The concordance rate for Monozygotic twins was 68% while it was 36% for Dizygotic twins. Children reared away from their parents are equally likely to develop the problem thus pointing towards a genitic basis for the disorder (Kaffman, 1962).
      Enuresis can represent a general neuromaturational delay or a specific developmental delay. There are many pointers towards a general immaturity of the nervous system in enuretic children. Children thus affected are more likely to show other developmental delays especially in speach and language and to a lesser extent motor delays (Shaffer 1984, Essen & Peckham, 1976).
      "Soft" neurological signs are "non-normative performance on a motor or sensory test identical to a test item of the traditional neurological examination, but a performance that is elicited". They include phenomena such as dysdiadochokinesis, mirror (contralateral) movements, dysgraphesthesia, astereognosis and the choreiform twitch. "Soft" signs can be reliably elicited (Rutter 1970). They may be developmental phenomena which are transient and disappear with neurological maturation. These signs have been described as occuring more frequently in groups of children with behaviour or learning problems than in "normal" children. The presence of these signs are thought to be due to evidence of immaturity of the nervous system.
      Shaeffer (1984) found that enuretic children had developemental delays, speech disfluency and soft neurological signs (scored using a routine neurological examination). In another study of 40 enuretic children between the ages of 7 and 13 years Mikkelsen et al (1980) found them to have higher scores on PANESS and were more psychiatrically disturbed. the physical and neurological examination of soft signs (PANESS) is a standardised examination procedure for elicitation of soft signs. It was initially described by Close (1973) and later modified by Denckle(1985). Enuretic children when compared with hyperkinetic and normal children show more soft signs (Mikkelsen et al, 1982). In these children, those with some psychiatric problem have more soft signs than those without. Using PANESS to elicit soft signs Kishor (1988) found that children with Primary Enuresis have more soft signs as compared with age and sex matched controls.
      Specific developmental delays associated with enuresis have already been described (speech and language, motor delays). There is some evidence which points towards enuresis being a specific developmental delay occuring in the cortical control of micturition. The evidence has come from urodynamic studies of those patients.
      Enuretics  are known to have smaller functional bladder capacities (Starfield,1967, Berg 1977, Kishore 1988) which is "the amount of urine a child would retain before expressing an urgent need to void".Functionally smaller bladders appear to be more characteristic of primary enuretics. Broughton and castan (1964) in a series of polygraphic sleep studies of enuresis, which included EEG patterns, measurement of intravesical pressures and EMG, came to the conclusion that enuretics have strong (of higher amplitude and frequency ) bladder contraction which are often not inhibited by subcortical centres. The "enuretic process" occurs during slow wavw sleep (stage 4 usually and is accompanied by strong bladder contraction pressures up to 100-120cm H2O) which is not inhibited by subcortical centres. The primary problem could thus be in an individual susceptibility to the peripheral reflex or some other biological handicap more centrally in the nervous system. Urologists have long felt that one of the basic abnormalities seen in the Enuretics is " detrussor hyperflexia" . This essentially means an unstable, over excitable bladder ( detrusor). It has been postulated that enuretics have a mild compensated form of detrusor hyperflexia(Mahoney et al 1980). Normal adults and children use the external sphicncter to control reflex bladder activity. Volitional constrant of micturition is done by contraction of the external sphincter and pelvic floor. In them voluntary facilitation is required to initiate detrusor contractions. In enuretics voluntary inhibition is required to prevent detrusor contractions (which keep occurring due to detrusor hyperflexia).

Enuretics are also characterised by two other deficits. The first is poor ceribral appreciation of bladder filling or contractions. (McGuire et al 1984). The second is a sacral neurological deficit, both sensory and motor. This more specifically is a deficit of the sacral reflex (measured by stimulation of the dorsal nerve of the penis/clitoris and noting reflex latencies) (Fidas et al 1985). Both could be due to neuromaturational delay (Fidas et al 1985).

  Thus to restate briefly, the evidence towards enuresis being a Neurodevelopmental disorder comes from
a) The evidence of genetic factors playing a definite role
b) The higher incidence of general neurodevelopmental problems (speach and Language) in enuretics
c) The presence of " Soft Neurologicalsigns"
d) Bladder instability , smaller functional urinary bladder, with poor cerebral appreciation fo bladder events and a sacral neural deficit.
    How does this help our understanding the problem and helping such patients ?. The very knowledge that the problem is self limiting usually helps.  Bladder training exercise aimed at strengthening voluntary controll is perhaps the most specific treatment