Areas of the skull that are covered with muscle have no underlying diploë formation between the internal and external lamina, which results in thin bone more susceptible to fractures.Skull fractures occur more easily at the thin squamous temporal and parietal bones, the sphenoid sinus, the foramen magnum (the opening at the base of the skull that the spinal cord passes through), the petrous temporal ridge, and the inner portions of the sphenoid wings at the base of the skull. The middle cranial fossa, a depression at the base of the cranial cavity forms the thinnest part of the skull and is thus the weakest part. This area of the cranial floor is weakened further by the presence of multiple foramina; as a result this section is at higher risk for basilar skull fractures to occur. Other areas more susceptible to fractures are the cribriform plate, the roof of orbits in the anterior cranial fossa, and the areas between the mastoid and dural sinuses in the posterior cranial fossa. Prognosis
Children with a simple skull fracture without other concerns are at low risk of a bad outcome and rarely require aggressive treatment.The presence of a concussion or skull fracture in people after trauma without intracranial hemorrhage or focal neurologic deficits was indicated in long term cognitive impairments and emotional lability at nearly double the rate as those patients without either complication.Those with a skull fracture were shown to have "neuropsychological dysfunction, even in the absence of intracranial pathology or more severe disturbance of consciousness on the GCS".
Neuronal ceroid lipofuscinosis  is the general name for a family of at least eight genetically separate neurodegenerative lysosomal storage diseases that result from excessive accumulation of lipopigments (lipofuscin) in the bodys tissues. These lipopigments are made up of fats and proteins. Their name comes from the word stem "lipo-", which is a variation on lipid, and from the term "pigment", used because the substances take on a greenish-yellow color when viewed under an ultraviolet light microscope. These lipofuscin materials build up in neuronal cells and many organs, including the liver, spleen, myocardium, and kidneys. Signs and symptoms
The classic characterization of the group of neurodegenerative, lysosomal storage disorders called the neuronal ceroid lipofuscinoses (NCLs) is through the progressive, permanent loss of motor and psychological ability with a severe intracellular accumulation of lipofuscins, with the United States and Northern European populations having slightly higher frequency with an occurrence of one in 10,000. Four classic diagnoses have received the most attention from researchers and the medical field, differentiated from one another by age of symptomatic onset, duration, early-onset manifestations such as blindness or seizures, and the forms which lipofuscin accumulation takes.In the early infantile variant of NCL (also called INCL or Santavuori-Haltia), probands appear normal at birth, but early visual loss leading to complete retinal blindness by the age of 2 years is the first indicator of the disease; by 3 years of age, a vegetative state is reached, and by 4 years, isoelectric encephalograms confirm brain death.