راهکارهای درمانی خاص در درمان لکنت زبان کلینیک تخصصی لکنت کرج جاده ملارد- جنب مجتمع مسکونی نیروگاه
alternatively, there is some predisposition toward a psychological profile that is consistent with stuttering, or a central nervous system which is conditioned toward reduced hemispheric dominance for speech and language? There is very little data in this area. However, one study (Janssen, Kraaimaat, & Brutten, 1990) found that a group of people who stuttered and had a family history of stuttering responded similarly when tested across a number of linguistic and psychological variables to a group who had no family history of stuttering. Interestingly though, those with a family history group showed more motoric disruptions in the form of blocks and prolongations than the no-history group. This finding may be seen tentatively to support the notion that genetic predisposition might directly implicate physiological functioning. However, as we continue to argue through the book, many variables associated with stuttering interrelate, making interpretation of findings more difficult.
Finally, clinicians accessing a young child with a stutter cannot access their own twin study data, but they can and often do conduct interviews in an attempt to establish a family history of stuttering. When taken as one of a number of indicators as to the multifactorial background to the disorder that we advocate is so important, this practice seems not just reasonable, but indeed, desirable. However, Felsenfeld (1998) pleads the case for restraint in assigning too much predictive power to this procedure in the strongest possible terms:
Family history (and recovery) status are complex noncategorical phe-nomena. Consequently, it must be understood that our attempts to establish “family history” in the clinic through a cursory interview are of questionable sensitivity and are almost certainly inaccurate. Although I am not suggesting that clinicians should stop collecting family history data during assessments, I am arguing that clinical decisions that are based in large part on these constituents should be avoided until we have stronger empirical evidence to support their predictive value. We know precious little about the genetic diathesis, and even less about the “stressors” that we know must be relevant for this diathesis to be activated.