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This paper deals with the diseases of Christiane, Goethe's wife, during the period of their marriage (1806-1816). Recurrent stomach complaints, due perhaps to gastro-duodenitis or an ulcer, were, it is suggested, of psychosomatic origin. They might have resulted from an intrinsic conflict between Christiane's unsatisfied desire for nearness and Goethe's absolute insistence on periods of distance and seclusion for the sake of his creative work. In contrast to this, Christiane's final illness was organic in nature. Contemporary records clearly indicate that she was suffering, not from suspected cerebrovascular accidents, but from the late form of symptomatic epilepsy with single grand mal seizures documented in 1815. In May/June 1816 these gave way to a series of grand mal seizures continuing into a malignant grand mal state, from which she never recovered. Pathogenetic aspects of the disease, allowing for the hypothesis of a latent infantile cerebral paresis together with the proven alcohol consumption are discussed and, in particular, the reasons why the correct diagnosis has been missed by posterity, even though it was clearly pointed out by Möbius as long ago as 1903. It is suggested that persistent irrational and unobjective prejudices relating to epilepsy, to Christiane's personality and last but not least to Möbius' pathographic approach have, up to the present, led to a dismissal of the true diagnosis of Christiane v. Goethe's final illness.

This paper presents an account of chronic-progressive Spinobulbar Spasticity (SBS) or Primary Lateral Sclerosis (PLS), a rare syndrome involving degeneration of the upper motoneuron, on the basis of 6 clinically examined cases. Individuals of both sexes can be affected. Onset of the syndrome occurs around the age of 54, but may sometimes be before 50. Early symptoms of the disease are spasticity on one leg and disturbance of motor skills in one hand. The symptoms generalize within two to three years into tetraspasticity accentuated in the legs, accompanied by pseudo-bulbar dysarthria and dysphagia, which, however, may also be present at the onset of the disease. Compulsive laughing and crying, optokinetic disturbances and facial stiffness develop as additional, though inconstant symptoms. Disease courses of 25 years were observed. Therapy is symptomatic. Fasciculation and muscular atrophy, which would indicate a transition to Amyotrophic Lateral Sclerosis (ALS), were not observed even if the disease was of longstanding. SBS differs from spastic spinal paralysis by virtue of its greater mean age of incidence, its tetraspasticity in conjunction with pseudobulbar signs, and-so far as can be established to date-its apparent non-hereditariness. An influence of exotoxic factors has not been demonstrated so far. The clinical syndrome results from a selective degeneration of the corticospinal and cortico-bulbar tracts up to the motor cortex, where loss of original pyramidal cells has been shown to occur (Pringle et al., 1992). The paper includes a survey of the clinical and neuropathological findings in cases of SBS published so far. Extensive anamnestic and clinical records including TCMS-studies, PET and NMR-CT scans performed in the parasagittal plane are essential for early diagnosis of the syndrome.