The radiological examinations usually demonstrate no abnormalities of the brain parenchyma.

In its early stage, CT scanning demonstrates no abnormalities. But by contrast scanning, linear enhancement of meninges sometimes can be demonstrated. By MR imaging, the meninges and brain surface are demonstrated with diffuse linear long or equal T₁ signal and long T₂ signal. The meningeal lesions are generally more serious at the base of brain, which can be demonstrated with obvious enhancement by contrast imaging (Fig. 23.5). There are also demonstrations of swollen adjacent brain tissues, enlarged and widened cisterns and sulci, and increased signal strength of cerebrospinal fluid. Due to accumulated and increased inflammatory exudates at the base of brain, communicating hydrocephalus commonly occurs. The meningeal lesions can disseminate along the cranial nerves at the base of brain to invade the cranial nerves, with common involvement of VII and VIII cranial nerves. Syphilitic myelitis is demonstrated as long T₁ long T₂ signals of the involved spinal cords. By contrast imaging, uneven enhancement can be demonstrated (Figs. 23.6 and 23.7). Due to common involvement of the meninges, the condition is also known as syphilitic meningomyelitis, manifested as inflammatory thickening of dura matter and its adhesion with pia matter of arachnoid membrane. The condition may further develop to cause lesions at the supplying vascular vessels and the nerve roots of the spinal cords, leading to spinal cord degeneration.

Meningovascular syphilis is pathologically characterized by proliferation of arteriolar endothelial cells and fibrocytes, thickening of vascular walls, stenosis, and blockage of the vascular lumen. After formation of cerebral infarction, MR imaging demonstrates typical T₁WI low signal and T₂WI high signal. By contrast imaging, the lesions are demonstrated with patches and cortical gyrus-like enhancement. After occurrence of encephalomalacia, the signal is the same as that of the cerebrospinal fluid.

Brain parenchymal syphilis includes paralytic dementia and myelophthisis. In the early stage of brain parenchymal syphilis, CT scanning demonstrates extensive low-density change, with accompanying edema. In the advanced stage of brain parenchyma syphilis, the cortex is subject to diffuse atrophy and expanded lateral ventricles, but no ischemia and inflammatory changes. T₁WI and T₂WI of MR imaging demonstrate atrophy of different degrees at bilateral frontal and temporal lobes that is more obvious at the anterior parts, bilaterally symmetric dilation of brain ventricles, and glial proliferation of subcortex and hippocampus (Fig. 23.8).

Gumma neurosyphilis can be found at any part of brain tissues, mostly at the cerebral cortex and subcortex. The round-like lesions may be singular or multiple, with a diameter of 2–2.5 cm. By T1WI, the central caseous necrosis of the lesion is demonstrated as low signal or equal low mixed signal, with surrounding low signal due to a large area of edema that shows space-occupying effect. By contrast imaging, the lesions are demonstrated with irregular ring-shaped enhancement and adjacent meningeal enhancement that indicates meningeal involvement Fig. 23.9. Intramedullary gumma neurosyphilis is manifested as swollen and thickened spinal cord, round-like or nodular lump that resembles to intracranial gumma, as well as enhancement and thickening of adjacent meninges.

Syphilitic aortitis is commonly complicated by incomplete closure of aortic valve, stenosis of coronary orifice, and other conditions. Ultrasonocardiography demonstrates dilated aorta, aortic regurgitation, and enlarged left ventricle.