The procedural memory system is associated with basal-ganglia circuits in the frontal lobe and further investigation of this particular hypothesis could aid in the development of a clinical neurological picture of what the underlying causes of SLI are. Scientific studies of speech and language
Some of the earliest neuroscientific discoveries were related to the discovery that damage to certain areas of the brain related to impairments in language, such as the discovery of Wernickes area and Brocas area. Lesions in these parts of the brain impair language comprehension and language production, respectively. Paul Broca was the first to note that the left hemisphere of the brain appeared to be localized for language function, particularly for right handed patients. Modern neuroscientific research has verified this, though language may be lateralizaed to the right hemisphere in some right-handed individuals. Developmental verbal dyspraxia
In 1990, it was reported that the several generations of the KE family had developmental verbal dyspraxia and orofacial praxis that were inherited in a typical autosomal dominant pattern. Further analysis traced this inheritance pattern back to mutations in the FOXP2 genes. These studies have allowed scientists to begin to investigate how changes to one gene can alter human communication. FOXP2 is the first gene that has been identified that is specifically linked to speech and language production. Mutant alleles of the normal FOXP2 gene have been found to be the cause of severe speech impairments. Specific language impairment
Neuroimaging techniques, such as structural and functional MRI, found no significant differences between individuals with SLI and normal controls.
Lethal arthrogryposis with anterior horn cell disease (LAAHD)  is an autosomal recessive genetic disorder characterized by reduced mobility of the foetus and early death. Presentation
LAAHD resembles LCCS1 disease but the phenotype is milder, with survival beyond 32nd gestational week. However, the foetuses are often stillborn or survive only few minutes. The movements of the foetus during pregnancy are scanty and stiff, often only in upper limbs. The malpositions are distal. The inwards spiral and especially the elbow contractures are less severe than in LCCS1 disease. Some patients have intrauterine long bone fractures. Skeletal muscles are affected and show neurogenic atrophy. The size and shape of spinal cord at different levels are normal but anterior horn motoneurons are diminished in number and degenerated. Molecular genetics
LAAHD disease results from compound heterozygosity of GLE1FinMajor and a missense point mutation in exon 13 (6 cases in 3 families) or a missense mutation in exon 16 ( seven cases in 3 families). One of the latter cases survived 12 weeks, mostly under artificial respiration. Diagnosis
Treatment
Epidemiology
LAAHD is one of approximately 40 Finnish heritage diseases. Families affected by these diseases come from different parts of Finland, and birthplaces of the ancestors of affected individuals do not show geographic clustering. References


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