Quadrantanopia refers to an anopia affecting a quarter of the field of vision. While quadrantanopia can be caused by lesions in the temporal and parietal lobes, it is most commonly associated with lesions in the occipital lobe.
A lesion affecting one side of the temporal lobe may cause damage to the inferior optic radiations (known as the temporal pathway or Meyer’s loop) which can lead to superior quadrantanopia on the contralateral side of both eyes (colloquially referred to as pie in the sky).

Therefore, a left temporal lobe infarct will affect the right superior quadrantanopia.

Nimodipine, a calcium-channel antagonist with a relatively selective vasodilatory effect on cerebral blood vessels, has been approved for improvement of neurologic deficits due to spasm following subarachnoid haemorrhage. Oral nimodipine is the most studied calcium channel blocker for prevention of vasospasm after Subarachnoid haemorrhage.
An American Heart Association/American Stroke Association guideline recommends its use for this purpose (class I, level of evidence A). Calcium channel blockers have been shown to reduce the incidence of ischemic neurologic deficits, and nimodipine has been shown to improve overall outcome within 3 months of aneurysmal SAH. Calcium channel blockers and other antihypertensives should be used cautiously to avoid the deleterious effects of hypotension.

The term subarachnoid haemorrhage (SAH) refers to extravasation of blood into the subarachnoid space between the pial and arachnoid membranes. SAH constitutes half of all spontaneous atraumatic intracranial haemorrhages; the other half consists of bleeding that occurs within the brain parenchyma.
Intracranial saccular aneurysms (“berry aneurysms”) represent the most common aetiology of nontraumatic SAH; about 80% of cases of SAH result from ruptured aneurysms.

This is a case of diffuse axonal injury (DAI) which occurs when the head is rapidly accelerated or decelerated.

DAI is a form of traumatic brain injury which occurs when the brain rapidly shifts inside the skull as an injury is occurring. The long connecting fibres in the brain called axons are sheared as the brain rapidly accelerates and decelerates inside the hard bone of the skull. There are two components of DAI:
1. Multiple haemorrhages
2. Diffuse axonal damage in the white matter

Up to two-thirds of the changes occurs at the junction of the grey and white matter due to the different densities of the tissue. These are mainly histological and axonal damage is secondary to biochemical cascades. Often, there are no signs of a fracture or contusion. DAI typically causes widespread injury to the brain leading to loss of consciousness. The changes in the brain are often very tiny and can be difficult to detect using CT or MRI scans.

The presence of blown right pupil is a sign of the third cranial nerve compression. The most likely cause is an extradural bleed. However, since this option is not listed, transtentorial herniation would be the most applicable answer. Intraventricular bleeds are typically more common in premature neonates and deterioration due to hydrocephalus is more chronic. Subdural haematoma has a slower onset of symptoms.

Transtentorial herniation is a type of cerebral herniaton. It is further divided into two types with the uncal herniation being the most common.
1. Descending transtentorial herniation: more frequently known as uncal herniation
2. Ascending transtentorial herniation: less common than uncal herniation

Uncal (transtentorial) herniation is herniation of the medial temporal lobe from the middle into the posterior fossa, across the tentorial opening. The cardinal signs are an acute loss of consciousness associated with ipsilateral oculomotor nerve palsy with a fixed and dilated pupil (blown pupil) and contralateral hemiparesis.

Germinal matrix/intraventricular haemorrhage (GM/IVH) is a complication of premature delivery that can result in life-long medical and developmental consequences. Although GM/IVH can occur in term infants, haemorrhage in this group of infants remains distinct from periventricular haemorrhage (PVH)/IVH of the preterm infant. Several acquired lesions of the central nervous system (CNS) specifically affect infants born prematurely and result in long-term disability, including GM/IVH, periventricular white matter injury (e.g., cystic periventricular leukomalacia [CPVL], periventricular haemorrhagic infarction [PVHI]), haemorrhage, and diffuse injury to the developing brain.
The physical examination is usually negative in germinal matrix/intraventricular haemorrhage (GM/IVH). Occasionally, severe GM/IVH may present with nonspecific systemic findings suggestive of cardiovascular collapse.

One subgroup of infants with GM/IVH presents with the following:
– A sudden unexplained drop in haematocrit levels
– Possible physical findings related to anaemia (e.g., pallor, poor perfusion) or haemorrhagic shock

Another subgroup of infants with GM/IVH presents with extreme signs, including the following:
– A sudden and significant clinical deterioration associated with anaemia, metabolic acidosis, glucose instability, respiratory acidosis, apnoea, hypotonia, and stupor is present.

Physical findings related to these signs include poor perfusion, pallor or an ashen colour, irregularities of respiratory pattern, signs of respiratory distress including retractions and tachypnoea, hypotonia, and altered mental status (e.g., decreased responsiveness, coma).

Additional neurologic signs, such as fullness of the fontanelles, seizures, and posturing, may also be observed. Progression can be rapid and may result in shock and death.

Extradural haemorrhage also known as an epidural hematoma, is a collection of blood that forms between the inner surface of the skull and outer layer of the dura, which is called the endosteal layer. They are usually associated with a history of head trauma and frequently associated skull fracture. The source of bleeding is usually arterial, most commonly from a torn middle meningeal artery.

A subdural haemorrhage (or hematoma) is a type of bleeding that often occurs outside the brain as a result of a severe head injury. It takes place when blood vessels burst between the brain and the leather-like membrane that wraps around the brain (the dura mater). The pooling blood creates pressure on the surface of the brain, causing a variety of problems.

Effective management of intracranial hypertension involves meticulous avoidance of factors that precipitate or aggravate increased intracranial pressure. When intracranial pressure becomes elevated, it is important to rule out new mass lesions that should be surgically evacuated. Medical management of increased intracranial pressure should include sedation, drainage of cerebrospinal fluid, and osmotherapy with either mannitol or hypertonic saline. For intracranial hypertension refractory to initial medical management, barbiturate coma, hypothermia, or decompressive craniectomy should be considered. Steroids are not indicated and may be harmful in the treatment of intracranial hypertension resulting from traumatic brain injury.
Mannitol is the most commonly used hyperosmolar agent for the treatment of intracranial hypertension.
Intravenous bolus administration of mannitol lowers the ICP in 1 to 5 minutes with a peak effect at 20 to 60 minutes. The effect of mannitol on ICP lasts 1.5 to 6 hours, depending on the clinical condition. Mannitol usually is given as a bolus of 0.25 g/kg to 1 g/kg body weight; when an urgent reduction of ICP is needed, an initial dose of 1 g/kg body weight should be given. Arterial hypotension (systolic blood pressure < 90 mm Hg ) should be avoided.

Lacunar stroke or lacunar infarct (LACI) is the most common type of ischaemic stroke, and results from the occlusion of small penetrating arteries that provide blood to the brain’s deep structures.

Types:
Pure motor stroke/hemiparesis – It is marked by hemiparesis or hemiplegia that typically affects the face, arm, or leg of the side of the body opposite the location of the infarct. Dysarthria, dysphagia, and transient sensory symptoms may also be present.

Ataxic hemiparesis – It displays a combination of cerebellar and motor symptoms, including weakness and clumsiness, on the ipsilateral side of the body. It usually affects the leg more than it does the arm; hence, it is known also as homolateral ataxia and crural paresis. The onset of symptoms is often over hours or days.

Dysarthria/clumsy hand – The main symptoms are dysarthria and clumsiness (i.e., weakness) of the hand, which often are most prominent when the patient is writing.

Pure sensory stroke – Marked by numbness (loss of sensation) on one side of the body; can later develop tingling, pain, burning, or another unpleasant sensation on one side of the body.

Mixed sensorimotor stroke – This lacunar syndrome involves hemiparesis or hemiplegia (weakness) with sensory impairment in the contralateral side.

Epidural hematoma (EDH) is a traumatic accumulation of blood between the inner table of the skull and the stripped-off dural membrane. EDH results from a traumatic head injury, usually with an associated skull fracture and arterial laceration. The inciting event often is a focused blow to the head, such as that produced by a hammer or baseball bat. In 85-95% of patients, this type of trauma results in an overlying fracture of the skull. Blood vessels in close proximity to the fracture are the sources of the haemorrhage in the formation of an epidural hematoma. Because the underlying brain has usually been minimally injured, prognosis is excellent if treated aggressively. Outcome from surgical decompression and repair is related directly to patient’s preoperative neurologic condition.

This patient may well develop raised ICP over the next few days and intracranial pressure monitoring will help with the
management.

Summary of guidelines:

For adults who have sustained a head injury and have any of the following risk factors, perform a CT head scan within 1 hour of the risk factor being identified:
– GCS less than 13 on initial assessment in the emergency department.
– GCS less than 15 at 2 hours after the injury on assessment in the emergency department.
– Suspected open or depressed skull fracture.
– Any sign of basal skull fracture (haemotympanum, ‘panda’ eyes, cerebrospinal fluid leakage from the ear or nose, Battle’s sign).
– Post-traumatic seizure.
– Focal neurological deficit.
– More than 1 episode of vomiting.
A provisional written radiology report should be made available within 1 hour of the scan being performed

For adults with any of the following risk factors who have experienced some loss of consciousness or amnesia since the injury, perform a CT head scan within 8 hours of the head injury:
– Age 65 years or older.
– Any history of bleeding or clotting disorders.
– Dangerous mechanism of injury (a pedestrian or cyclist struck by a motor vehicle, an occupant ejected from a motor vehicle or a fall from a height of greater than 1 metre or 5 stairs).
– More than 30 minutes’ retrograde amnesia of events immediately before the head injury.
A provisional written radiology report should be made available within 1 hour of the scan being performed.

– Intubate and ventilate all patients with GCS 8 or less requiring transfer to a neuroscience unit.
Intubate and ventilate the patient immediately in the following circumstances:
– Coma – not obeying commands, not speaking, not eye opening (that is, GCS 8 or less).
– Loss of protective laryngeal reflexes.
– Ventilatory insufficiency as judged by blood gases: hypoxaemia (PaO2 < 13 kPa on oxygen) or hypercarbia (PaCO2 > 6 kPa).
– Spontaneous hyperventilation causing PaCO2 < 4 kPa.
– Irregular respirations.

Use the criteria below for admitting patients to hospital following a head injury:
– Patients with new, clinically significant abnormalities on imaging.
– Patients whose GCS has not returned to 15 after imaging, regardless of the imaging results.
– When a patient has indications for CT scanning but this cannot be done within the appropriate period, either because CT is not available or because the patient is not sufficiently cooperative to allow scanning.
– Continuing worrying signs (for example, persistent vomiting, severe headaches) of concern to the clinician.
– Other sources of concern to the clinician (for example, drug or alcohol intoxication, other injuries, shock, suspected non-accidental injury, meningism, cerebrospinal fluid leak).
– Perform and record observations on a half-hourly basis until GCS equal to 15 has been achieved.
– Do not discharge patients presenting with head injury until they have achieved GCS equal to 15

Answer: Acute subdural haematoma

An acute subdural haematoma (SDH) is a clot of blood that develops between the surface of the brain and the dura mater, the brain’s tough outer covering, usually due to stretching and tearing of veins on the brain’s surface. These veins rupture when a head injury suddenly jolts or shakes the brain.
Traumatic acute SDHs are among the most lethal of all head injuries. Associated with more severe generalized brain injury, they often occur with cerebral contusions.
SDHs are seen in 10 percent to 20 percent of all traumatic brain injury cases and occur in up to 30 percent of fatal injuries.
Diagnosis:

SDHs are best diagnosed by computed tomography (CT) scan. They appear as a dense, crescent-shaped mass over a portion of the brain’s surface.
Most patients with acute SDHs have low Glasgow Coma Scale (GCS) scores on admission to the hospital.

Acute traumatic subdural haematoma often results from falls, violence, or motor vehicle accidents. Suspect acute subdural haematoma whenever the patient has experienced moderately severe to severe blunt head trauma. The clinical presentation depends on the location of the lesion and the rate at which it develops. Often, patients are rendered comatose at the time of the injury. A subset of patients remain conscious; others deteriorate in a delayed fashion as the haematoma expands.
A GCS score less than 15 after blunt head trauma in a patient with no intoxicating substance use (or impaired mental status baseline) warrants consideration of an urgent CT scan. Search for any focal neurologic deficits or signs of increased ICP. Any abnormality of mental status that cannot be explained completely by alcohol intoxication or the presence of another mind-altering substance should increase suspicion of subdural hematoma in the patient with blunt head trauma.

The clinical presentation of a patient with an acute subdural haematoma depends on the size of the hematoma and the degree of any associated parenchymal brain injury. Symptoms associated with acute subdural haematoma include the following:

Headache

Nausea

Confusion

Personality change

Decreased level of consciousness

Speech difficulties

Other change in mental status

Impaired vision or double vision

Weakness

On noncontrast CT scan, an acute subdural haematoma appears as a hyperdense (white), crescent-shaped mass between the inner table of the skull and the surface of the cerebral hemisphere.

Acute subdural hematoma is usually caused by external trauma that creates tension in the wall of a bridging vein as it passes between the arachnoid and dural layers of the brain’s lining—i.e., the subdural space. The circumferential arrangement of collagen surrounding the vein makes it susceptible to such tearing.

Acute bleeds often develop after high-speed acceleration or deceleration injuries. They are most severe if associated with cerebral contusions. Though much faster than chronic subdural bleeds, acute subdural bleeding is usually venous and therefore slower than the arterial bleeding of an epidural haemorrhage. Acute subdural hematomas due to trauma are the most lethal of all head injuries and have a high mortality rate if they are not rapidly treated with surgical decompression. The mortality rate is higher than that of epidural hematomas and diffuse brain injuries because the force required to cause subdural hematomas tends to cause other severe injuries as well.

Generally, acute subdural hematomas are less than 72 hours old and are hyperdense compared with the brain on computed tomography scans. The subacute phase begins 3-7 days after acute injury. Chronic subdural hematomas develop over the course of weeks and are hypodense compared with the brain. However, subdural hematomas may be mixed in nature, such as when acute bleeding has occurred into a chronic subdural hematoma.
Lateralizing findings include ipsilateral pupillary dilatation with impaired reaction and motor deficit. Usually the pupillary dilatation will be ipsilateral and motor deficit (hemiparesis or hemiplegia) will be contralateral to the site of subdural hematoma.

Risk of haematoma (requiring removal) in adults attending accident and emergency units following head injury.

Risk Factor Risk of haematoma
Oriented, no skull fracture 1 in 5983
Not oriented, no skull fracture 1 in 121
Skull fracture, Orientated 1 in 32
Skull fracture, Not orientated 1 in 4

The classic symptom of subarachnoid haemorrhage is thunderclap headache (a headache described as like being kicked in the head, or the worst ever, developing over seconds to minutes). This headache often pulsates towards the occiput (the back of the head). About one-third of people have no symptoms apart from the characteristic headache, and about one in ten people who seek medical care with this symptom are later diagnosed with a subarachnoid haemorrhage. Vomiting may be present, and 1 in 14 have seizures. Confusion, decreased level of consciousness or coma may be present, as may neck stiffness and other signs of meningism.
In 85 percent of spontaneous cases the cause is a cerebral aneurysm—a weakness in the wall of one of the arteries in the brain that becomes enlarged. They tend to be located in the circle of Willis and its branches. While most cases are due to bleeding from small aneurysms, larger aneurysms (which are less common) are more likely to rupture. Aspirin also appears to increase the risk.
In 15–20 percent of cases of spontaneous SAH, no aneurysm is detected on the first angiogram. About half of these are attributed to non-aneurysmal perimesencephalic haemorrhage, in which the blood is limited to the subarachnoid spaces around the midbrain (i.e. mesencephalon). In these, the origin of the blood is uncertain. The remainder are due to other disorders affecting the blood vessels (such as cerebral arteriovenous malformations), disorders of the blood vessels in the spinal cord, and bleeding into various tumours.
Genetics may play a role in a person’s disposition to SAH; risk is increased three- to fivefold in first-degree relatives of people having had a subarachnoid haemorrhage. But lifestyle factors are more important in determining overall risk. These risk factors are smoking, hypertension (high blood pressure), and excessive alcohol consumption.
The absence of trauma and skull fracture rules out the other types of haemorrhages and haematomas.

von Hippel-Lindau (VHL) disease, or von Hippel-Lindau syndrome, is a rare genetic disorder characterized by visceral cysts and benign tumours in multiple organ systems that have a subsequent potential for malignant change.
Clinical hallmarks of VHL disease include the development of retinal and central nervous system (CNS) hemangioblastomas (blood vessel tumours), pheochromocytomas, multiple cysts in the pancreas and kidneys, and an increased risk for malignant transformation of renal cysts into renal cell carcinoma. The wide age range and the pleiotropic manner in which VHL disease presents complicates diagnosis and treatment in affected individuals, as well as their at-risk relatives.

Because VHL disease is a multiple-organ disease that widely varies in clinical presentation, various manifestations may lead to the diagnosis. Criteria are the following:
More than one hemangioblastoma in the CNS (brain, spinal cord) or eye
A single hemangioblastoma in the CNS or retina, plus a visceral manifestation (multiple renal, pancreatic, or hepatic cysts; pheochromocytoma; renal cancer)
Positive family history plus any one of the above clinical manifestations
Elucidation of a deleterious mutation in the VHL gene