While decorticate posturing is still an ominous sign of severe brain damage, decerebrate posturing is usually indicative of more severe damage at the rubrospinal tract, and hence, the red nucleus is also involved, indicating a lesion lower in the brainstem. Decerebrate
Decerebrate posturing is also called decerebrate response, decerebrate rigidity, or extensor posturing. It describes the involuntary extension of the upper extremities in response to external stimuli. In decerebrate posturing, the head is arched back, the arms are extended by the sides, and the legs are extended. A hallmark of decerebrate posturing is extended elbows. The arms and legs are extended and rotated internally. The patient is rigid, with the teeth clenched. The signs can be present on only one side of the body or on both sides, and they may be present just in the arms, and they may be intermittent.A person displaying decerebrate posturing in response to pain receives a score of two in the motor section of the Glasgow Coma Scale (for adults) and the Pediatric Glasgow Coma Scale (for infants), due to the muscles extending because of the neuro-muscular response to the trauma.Decerebrate posturing indicates brain stem damage, specifically damage below the level of the red nucleus (e.g. mid-collicular lesion). It is exhibited by people with lesions or compression in the midbrain and lesions in the cerebellum. Decerebrate posturing is commonly seen in pontine strokes. A patient with decorticate posturing may begin to show decerebrate posturing, or may go from one form of posturing to the other.
Hypogonadism, kidney failure, urogenital sinuses, ectopic urethra, uterus duplex, septate vagina, and hypoplasia of the uterus, ovaries, and fallopian tubes
Speech disorder/delay
Developmental delay, especially of fine and gross motor skills

Relation to other rare genetic disorders
Findings in genetic research published in 2006 have suggested that a large number of genetic disorders, both genetic syndromes and genetic diseases, that were not previously identified in the medical literature as related, may be, in fact, highly related in the genetypical root cause of the widely varying, phenotypically observed disorders. BBS is one such syndrome that has now been identified to be caused by defects in the cellular ciliary structure. Thus, BBS is a ciliopathy. Other known ciliopathies include primary ciliary dyskinesia, polycystic kidney and liver disease, nephronophthisis, Alström syndrome, Meckel–Gruber syndrome and some forms of retinal degeneration. Pathophysiology
The detailed biochemical mechanism that leads to BBS is still unclear.The gene products encoded by these BBS genes, called BBS proteins, are located in the basal body and cilia of the cell.Using the round worm C. elegans as a model system, biologists found that BBS proteins are involved in a process called intraflagellar transport (IFT), a bi-directional transportation activity within the cilia along the long axis of the ciliary shaft that is essential for ciliogenesis and the maintenance of cilia. Recent biochemical analysis of human BBS proteins revealed that BBS proteins are assembled into a multiple protein complex, called "BBSome".