Cushings triad
Cushings triad is a clinical triad variably defined as having:

Irregular, decreased respirations (caused by impaired brainstem function)
Bradycardia
Systolic hypertension (widening pulse pressure)

History
Cushings reflex is named after Harvey Williams Cushing (1869–1939), an American neurosurgeon. Cushing began his research in Bern, Switzerland studying abroad with Emil Theodor Kocher. A month into his trip, Cushing received a formal proposition from Emil Theodor Kocher to begin testing how compression of the brain affected blood vessels. Cushing also enlisted the aid of Hugo Kronecker, a known blood pressure researcher. Utilizing Kroeneckers assistance and resources, Cushing began his research. Cushing left Bern in 1901 to work in Turin, Italy with Angelo Mosso, a previous student of Kroenecker. He continued to work on the same research project, while also simultaneously improving his methods of recording coincidence of blood pressure and ICP. In June 1901 Cushing published his first paper through Johns Hopkins Hospital Bulletin entitled "Concerning a definite regulatory mechanism of the vasomotor centre which controls blood pressure during cerebral compression". Between 1901 and 1903, Cushing published five papers pertaining to his research on the vasopressor response. These papers were published in German and English, and one was authored by Emil Theodor Kocher. Experimental setup and results
Cushing began experimenting once he obtained approval from Kocher. His experimental setup was a modified version of  Leonard Hills model to similarly test the effects of brain pressure on sinus pressure, cerebrospinal fluid pressure, arterial and venous blood pressure. Like Hill, Cushing used dogs for his experiments.
Individuals with this symptom of CBD often lose the ability to speak as the disease progresses. Psychiatric and cognitive disorders
Psychiatric problems associated with CBD often present as a result of the debilitating symptoms of the disease. Prominent psychiatric and cognitive conditions cited in individuals with CBD include dementia, depression, and irritability, with dementia forming a key feature that sometimes leads to the misdiagnosis of CBD as another cognitive disorder such as Alzheimers disease (AD). Frontotemporal dementia can be an early feature. Molecular features
Neuropathological findings associated with CBD include the presence of astrocytic abnormalities within the brain and improper accumulation of the protein tau (referred to as tauopathy). Astroglial inclusions
Postmortem histological examination of the brains of individuals diagnosed with CBD reveal unique characteristics involving the astrocytes in localized regions. The typical procedure used in the identification of these astroglial inclusions is the Gallyas-Braak staining method. This process involves exposing tissue samples to a silver staining material which marks for abnormalities in the tau protein and astroglial inclusions. Astroglial inclusions in CBD are identified as astrocytic plaques, which present as annularly displays of blurry outgrowths from the astrocyte. A recent study indicated that  produces a high density of astrocytic plaques in the anterior portion of the frontal lobe and in the premotor area of the cerebral cortex. Tauopathy
The protein tau is an important microtubule-associated protein (MAP), and is typically found in neuronal axons. However, malfunctioning of the development of the protein can result in unnatural, high-level expression in astrocytes and glial cells.