Neurological
Three types of brain tumours are associated with TSC:

Giant cell astrocytoma: (grows and blocks the cerebrospinal fluid  flow, leading to dilatation of ventricles causing headache and vomiting)
Cortical tubers: after which the disease is named
Subependymal nodules: form in the walls of ventriclesClassic intracranial manifestations of TSC include subependymal nodules and cortical/subcortical tubers.The tubers are typically triangular in configuration, with the apex pointed towards the ventricles, and are thought to represent foci of abnormal neuronal migration. The T2 signal abnormalities may subside in adulthood, but will still be visible on histopathological analysis. On magnetic resonance imaging (MRI), TSC patients can exhibit other signs consistent with abnormal neuron migration such as radial white matter tracts hyperintense on T2WI and heterotopic grey matter.Subependymal nodules are composed of abnormal, swollen glial cells and bizarre multinucleated cells which are indeterminate for glial or neuronal origin. Interposed neural tissue is not present. These nodules have a tendency to calcify as the patient ages. A nodule that markedly enhances and enlarges over time should be considered suspicious for transformation into a subependymal giant cell astrocytoma, which typically develops in the region of the foramen of Monro, in which case it is at risk of developing an obstructive hydrocephalus.A variable degree of ventricular enlargement is seen, either obstructive (e.g. by a subependymal nodule in the region of the foramen of Monro) or idiopathic in nature. Neuropsychiatric
About 90% of people with TSC develop a range of neurodevelopmental, behavioural, psychiatric, and psychosocial difficulties. The "TSC‐associated neuropsychiatric disorders" are abbreviated TAND.
Blood flow is selectively redirected to the myocardium, adrenal glands, and in particular to the brain in a brain-sparing effect.In late stage, the redistribution becomes ineffective, there is decrease in cardiac output, ineffective preload handling and elevation of central venous pressure. This deterioration in circulation may ultimately lead to tricuspid insufficiency and death of the fetus. Peripheral circulatory disturbances also accompany these central circulatory changes. Fetal behavioral changes
Chronic hypoxemia leads to delay in all aspects of CNS maturation. With worsening fetal hypoxemia, there is decline in fetal activity. With further hypoxemia, fetal breathing ceases. Gross body movements and tone decrease further. Fetal heart rate decreases due to spontaneous deceleration due to direct depression of cardiac contractility. This leads to intrauterine fetal death. Risk of later metabolic disease
According to the theory of thrifty phenotype, placental insufficiency triggers epigenetic responses in the fetus that are otherwise activated in times of chronic food shortage. If the offspring actually develops in an environment rich in food it may be more prone to metabolic disorders, such as obesity and type II diabetes.