RAMMOLLIMENTO CEREBRALE
The concept of cerebral softening (*rammollimento cerebrale*) is quite precise and well-defined from an anatomo-pathological standpoint, but much less so from a pathogenetic and clinical perspective. Cerebral softening refers to an alteration of the cerebral substance that appears in foci of varying size, sometimes single, more often multiple, and at times so widespread as to involve the entire brain.
Softening is not an alteration exclusive to the cerebral substance, as it can also affect other organs, and essentially consists of a focus of necrosis followed generally by a reparative process in which the destroyed cellular elements are eliminated and replaced by fibrous tissue. The site, size, singularity or multiplicity, and the stage—whether recent or late—at which it is observed render the picture of cerebral softening highly variable. A recent focus appears to the naked eye as an area of varying size with indistinct boundaries, of a whitish-yellow color (white softening or ischemic necrosis) or tending toward brown (red softening or hemorrhagic infarction), of soft consistency or otherwise diminished compared to the surrounding healthy tissue. The central part undergoes colliquation and softening, while at the periphery a fibrous-scar tissue forms that may surround and isolate the colliquated portion from the rest of the parenchyma (formation of a cyst), or eliminate it or replace it (sclerosis). Sclerosis represents the outcome of a reactive process of the supporting or glial tissue (glial reaction) in response to the softened area. Although the mechanism by which it forms remains a matter of debate, cerebral softening can, for simplicity’s sake, be attributed to a disturbance of the blood circulation that results in a diminished blood supply to the cerebral substance: the affected area suffers from the nutritional deficit and undergoes necrosis. For this reason, cerebral softening is characteristic of diseases affecting the cerebral vessels, particularly arteriosclerosis, of which it represents the most typical and overt manifestation.
Arteriosclerosis of the cerebral vessels consists of an alteration of the vascular walls that leads to the formation of islands of fatty substances (fatty degeneration), the deposition of calcium salts (atheromas), the loss of elastic tissue with secondary formation of connective tissue (sclerosis). The vessels become rigid and hard, their lumen increasingly narrowed by the superimposition of atheromatous plaques or by the formation of thrombi. The diminished blood supply to the cerebral parenchyma can be sudden and extensive (as in the thrombotic occlusion of a large artery), resulting in large softenings that affect broad areas of cerebral tissue, while the more or less complete and gradual occlusion of small vessels, sometimes diffused throughout the brain, leads to the formation of small, diffuse, multiple softenings, with small areas of atrophy around the vessels (lacunar state).
The clinical symptomatology is essentially neurological (see DISEASES, NERVOUS) and psychic; the latter is more pronounced and typical in the multiple softenings of generalized arteriosclerosis. The neurological symptoms are closely related to the site of the softening: epileptic seizures, hemiplegias, and aphasias are frequent. Very often the foci of softening are bilateral, and in such cases certain symptoms clearly indicative of a bilateral lesion appear, rendering the diagnosis highly probable. Among these are cited the amimic facies with spasmodic crying and laughing, disturbances of phonation and deglutition, and a gait consisting of small steps (pseudo-bulbar syndrome). These disturbances generally develop gradually and are subject to exacerbations and partial remissions.
The psychic symptomatology constitutes the picture of “arteriosclerotic dementia,” whose principal signs are hyperactivity and the decline of intellectual functions; the patient appears impressionable, irritable, prone to tears, frequently anxious and depressed, even in awareness of his condition. Immediate memory is selectively impaired, recent acquisitions are lost, while remote events may be recalled in minute detail.
Diagnosis generally presents no difficulty: the gradual onset (though not always) distinguishes a paralysis due to thrombotic softening from the sudden and dramatic ones caused by cerebral hemorrhages (apoplectic stroke). Arteriosclerotic dementia is distinguished from senile dementia by the simultaneous presence of neurological signs and because the latter presents with a global and uniform decline of all psychic functions.