An 87-year-old woman suffered a right frontal TBI when she accidentally fell in a nursing home. Her known medical history included mitral valve disease, episodes of paroxysmal atrial flutter and haemodynamic angina, and deep vein thrombosis with pulmonary thromboembolism. He was receiving drug treatment with Sintrom®, Acuprel®, Nitroplast®, Trangorex® and Diluton®.
As a result of the TBI there was a contused wound in the right ciliary region which was repaired with sutures. The following day, in a period of less than twelve hours, after starting her usual activities (toileting and breakfast), she experienced a progressive deterioration in her level of consciousness and anisocoria with mydriatic right pupil, for which she was transferred to the emergency department of the local hospital. On admission, Glasgow Glasgow 8-9 and anisocoria were noted. A cranial CT scan was performed (without contrast) which was reported as "chronic DHS with rebleeding" covering the right frontal, temporal and parietal regions; supracallosal and transstentorial herniation; and subarachnoid haemorrhage (SAH) in the right hemisphere. After her neurosurgical assessment, it was decided not to intervene and to transfer her back to her home, where she died fourteen hours later.

During the examination of the body we found the body of a woman of the aforementioned age. Numerous contusions at different stages of development were observed. The presence of a sutured wound with four stitches in the right ciliary region together with multiple contusions of different colours (reddish and bluish) close to it stands out due to its relation to the facts.
A judicial autopsy was carried out thirty-one hours after death. In the internal habitus, at the thoracoabdominal level, various macroscopic findings of interest were observed. The heart weighs 250 g and shows calcified atheroma plaques in the anterior descending and circumflex coronary arteries that reduce the lumen by > 90%, scars from old infarctions in the posterior wall of the left ventricle and papillary muscle, and calcification of the mitral annulus.
In the cranial cavity there is right frontotemporoparietal SDH consisting of dark coagulated blood with no evidence of associated fractures. The brain was fixed in formalin for 24 days before completing its macroscopic study, with the following findings: weight 1018 g and in addition to the described DHS, there was an external right subarachnoid haemorrhage; right trans-stentorial herniation furrow and haemorrhage in the midbrain. Coronal sections showed flattening of the right hemisphere, especially the frontal lobe, associated with a 15 mm thick subdural haematoma with a gelatinous appearance in the centre, with no evidence of neomembrane; midline deviation to the left, with collapse of the right lateral ventricle and dilatation of the left; supracallosal herniation and foci of haemorrhage in the right frontal white matter, corpus callosum, right thalamus and right frontal cortex. The midbrain shows extensive haemorrhage in the midline, right paramedial portion and dorsolateral quadrants and, in the pons, foci of haemorrhage can be seen in the floor of the fourth ventricle and cerebellar peduncles.

Samples of subdural haematoma, cortex and white matter from the right parasagittal frontal region, lenticular nucleus, internal capsule, thalamus, corpus callosum, hippocampus, midbrain, cerebellar peduncles, pons and bulb were taken for microscopic analysis.
Microscopic examination of the subdural haematoma shows that it consists of well-preserved red blood cells in the periphery and acellular proteinaceous material in the central areas. No haemosiderophages (Perls' stain is negative) and no signs of organisation on the arachnoid side (the dura mater was strongly adherent to the cranial calotte and was not removed for microscopic examination). Given the diagnostic disparity between the CT scan and the autopsy regarding the date of the HSD, the preparations corresponding to the haematoma were re-examined and arachnoid lining around the haematoma was identified in some areas.

In the brain parenchyma adjacent to the haematoma, glial cells with early reactive changes (globoid morphology with eosinophilic cytoplasm) were identified and oedema was observed around the foci of haemorrhage described. In the trunk, occasional axonal beads and spongiosis are observed around the haemorrhages.

Other neuropathological findings, compatible with the patient's age, were the presence of numerous senile plaques throughout the cortex, microcalcifications in the basal ganglia and hippocampus, and neurons with granulovacuolar and neurofibrillary degeneration in the hippocampus.
The chemical-toxicological analysis carried out at the INTCF (Dpto. of Madrid) on blood samples was negative for the toxins investigated (barbiturates, benzodiazepines, analgesics -paracetamol, metamizol, tramadol, salicylates-, antidepressants, phenothiazines and analogues, sulphonylurea-type antidiabetics, non-steroidal anti-inflammatory drugs, non-steroidal anti-inflammatory drugs, diuretics, xanthine bases, antiparkinsonian drugs, antihistamines, antihypertensives, antiplatelet agents, benzamides, morphine-derived opioids and ethyl alcohol).
Thus, we consider that the sequence of the lesions or pathology found would be as follows: an elderly person with a history of heart disease referred to above, on treatment with oral anticoagulants (Sintrom®), suffers a slight right frontoparietal trauma, which generates a rupture of a pre-existing arachnoid cyst and therefore an acute SDH, giving rise to intracranial hypertension, entrapment and death.
