Traumatic brain injury (TBI) is an exchangeable word used for the word concussion. This term refers to a mild brain injury. This injury is a result due to a blow to the head that could make the person’s physical, cognitive, and emotional behaviors irregular. Symptoms may include clumsiness, fatigue, confusion, nausea, blurry vision, headaches, and others. Mild concussions are associated with sequelae. Severity is measured using various concussion grading systems.

A slightly greater injury is associated with both anterograde and retrograde amnesia (inability to remember events before or after the injury). The amount of time that the amnesia is present correlates with the severity of the injury. In all cases the patients develop postconcussion syndrome, which includes memory problems, dizziness, tiredness, sickness and depression. Cerebral concussion is the most common head injury seen in children.

Diffuse axonal injury, or DAI, usually occurs as the result of an acceleration or deceleration motion, not necessarily an impact. Axons are stretched and damaged when parts of the brain of differing density slide over one another. Prognoses vary widely depending on the extent of damage.

Birth trauma (BT) refers to damage of the tissues and organs of a newly delivered child, often as a result of physical pressure or trauma during childbirth. The term also encompasses the long term consequences, often of a cognitive nature, of damage to the brain or cranium. Medical study of birth trauma dates to the 16th century, and the morphological consequences of mishandled delivery are described in Renaissance-era medical literature. Birth injury occupies a unique area of concern and study in the medical canon. In ICD-10 "birth trauma" occupied 49 individual codes (P10-Р15).

However, there are often clear distinctions to be made between brain damage caused by birth trauma and that induced by intrauterine asphyxia. It is also crucial to distinguish between "birth trauma" and "birth injury". Birth injuries encompass any systemic damages incurred during delivery (hypoxic, toxic, biochemical, infection factors, etc.), but "birth trauma" focuses largely on mechanical damage. Caput succedaneum, subcutaneous hemorrhages, small subperiostal hemorrhages, hemorrhages along the displacements of cranial bones, intradural bleedings, subcapsular haematomas of liver, are among the more commonly reported birth injuries. Birth trauma, on the other hand, encompasses the enduring side effects of physical birth injuries, including the ensuing compensatory and adaptive mechanisms and the development of pathological processes (pathogenesis) after the damage.

Pain, especially headache, is a common complication following a TBI. Being unconscious and lying still for long periods can cause blood clots to form (deep venous thrombosis), which can cause pulmonary embolism. Other serious complications for patients who are unconscious, in a coma, or in a vegetative state include pressure sores, pneumonia or other infections, and progressive multiple organ failure.

The risk of post-traumatic seizures increases with severity of trauma (image at right) and is particularly elevated with certain types of brain trauma such as cerebral contusions or hematomas. As many as 50% of people with penetrating head injuries will develop seizures. People with early seizures, those occurring within a week of injury, have an increased risk of post-traumatic epilepsy (recurrent seizures occurring more than a week after the initial trauma) though seizures can appear a decade or more after the initial injury and the common seizure type may also change over time. Generally, medical professionals use anticonvulsant medications to treat seizures in TBI patients within the first week of injury only and after that only if the seizures persist.

Neurostorms may occur after a severe TBI. The lower the Glasgow Coma Score (GCS), the higher the chance of Neurostorming. Neurostorms occur when the patient's Autonomic Nervous System (ANS), Central Nervous System (CNS), Sympathetic Nervous System (SNS), and ParaSympathetic Nervous System (PSNS) become severely compromised https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology . This in turn can create the following potential life-threatening symptoms: increased IntraCranial Pressure (ICP), tachycardia, tremors, seizures, fevers, increased blood pressure, increased Cerebral Spinal Fluid (CSF), and diaphoresis https://www.brainline.org/story/neurostorm-century-part-1-3-medical-terminology. A variety of medication may be used to help decrease or control Neurostorm episodes https://www.brainline.org/story/neurostorm-century-part-3-3-new-way-life.

Parkinson's disease and other motor problems as a result of TBI are rare but can occur. Parkinson's disease, a chronic and progressive disorder, may develop years after TBI as a result of damage to the basal ganglia. Other movement disorders that may develop after TBI include tremor, ataxia (uncoordinated muscle movements), and myoclonus (shock-like contractions of muscles).

Skull fractures can tear the meninges, the membranes that cover the brain, leading to leaks of cerebrospinal fluid (CSF). A tear between the dura and the arachnoid membranes, called a CSF fistula, can cause CSF to leak out of the subarachnoid space into the subdural space; this is called a subdural hygroma. CSF can also leak from the nose and the ear. These tears can also allow bacteria into the cavity, potentially causing infections such as meningitis. Pneumocephalus occurs when air enters the intracranial cavity and becomes trapped in the subarachnoid space. Infections within the intracranial cavity are a dangerous complication of TBI. They may occur outside of the dura mater, below the dura, below the arachnoid (meningitis), or within the brain itself (abscess). Most of these injuries develop within a few weeks of the initial trauma and result from skull fractures or penetrating injuries. Standard treatment involves antibiotics and sometimes surgery to remove the infected tissue.

Injuries to the base of the skull can damage nerves that emerge directly from the brain (cranial nerves). Cranial nerve damage may result in:

- Paralysis of facial muscles

- Damage to the nerves responsible for eye movements, which can cause double vision

- Damage to the nerves that provide sense of smell

- Loss of vision

- Loss of facial sensation

- Swallowing problems

Hydrocephalus, post-traumatic ventricular enlargement, occurs when CSF accumulates in the brain, resulting in dilation of the cerebral ventricles and an increase in ICP. This condition can develop during the acute stage of TBI or may not appear until later. Generally it occurs within the first year of the injury and is characterized by worsening neurological outcome, impaired consciousness, behavioral changes, ataxia (lack of coordination or balance), incontinence, or signs of elevated ICP.

Any damage to the head or brain usually results in some damage to the vascular system, which provides blood to the cells of the brain. The body can repair small blood vessels, but damage to larger ones can result in serious complications. Damage to one of the major arteries leading to the brain can cause a stroke, either through bleeding from the artery or through the formation of a blood clot at the site of injury, blocking blood flow to the brain. Blood clots also can develop in other parts of the head. Other types of vascular complications include vasospasm, in which blood vessels constrict and restrict blood flow, and the formation of aneurysms, in which the side of a blood vessel weakens and balloons out.

Fluid and hormonal imbalances can also complicate treatment. Hormonal problems can result from dysfunction of the pituitary, the thyroid, and other glands throughout the body. Two common hormonal complications of TBI are syndrome of inappropriate secretion of antidiuretic hormone and hypothyroidism.

Another common problem is spasticity. In this situation, certain muscles of the body are tight or hypertonic because they cannot fully relax.

While any number of injuries may occur during the birthing process. A number of specific conditions are well described. Brachial plexus palsy occurs in 0.4 to 5.1 infants per 1000 live birth. Head trauma and brain damage during delivery can lead to a number of conditions include: caput succedaneum, cephalohematoma, subgaleal hemorrhage, subdural hemorrhage, subarachnoid hemorrhage, epidural hemorrhage, and intraventricular hemorrhage.

The most common fracture during delivery is that of the clavicle (0.5%).

A skull fracture is a break in one or more of the eight bones that form the cranial portion of the skull, usually occurring as a result of blunt force trauma. If the force of the impact is excessive, the bone may fracture at or near the site of the impact and cause damage to the underlying physical structures contained within the skull such as the membranes, blood vessels, and brain.

While an uncomplicated skull fracture can occur without associated physical or neurological damage and is in itself usually not clinically significant, a fracture in healthy bone indicates that a substantial amount of force has been applied and increases the possibility of associated injury. Any significant blow to the head results in a concussion, with or without loss of consciousness.

A fracture in conjunction with an overlying laceration that tears the epidermis and the meninges, or runs through the paranasal sinuses and the middle ear structures, bringing the outside environment into contact with the cranial cavity is called a compound fracture. Compound fractures can either be clean or contaminated.

There are four major types of skull fractures:

- Linear

- Depressed

- Diastatic

- Basilar

Linear fractures are the most common, and usually require no intervention for the fracture itself. Depressed fractures are usually comminuted, with broken portions of bone displaced inward—and may require surgical intervention to repair underlying tissue damage. Diastatic fractures widen the sutures of the skull and usually affect children under three. Basilar fractures are in the bones at the base of the skull.

Basilar skull fractures are linear fractures that occur in the floor of the cranial vault (skull base), which require more force to cause than other areas of the neurocranium. Thus they are rare, occurring as the only fracture in only 4% of severe head injury patients.

Basilar fractures have characteristic signs: blood in the sinuses; a clear fluid called cerebrospinal fluid (CSF) leaking from the nose (rhinorrhea) or ears (otorrhea); periorbital ecchymosis often called 'raccoon eyes' (bruising of the orbits of the eyes that result from blood collecting there as it leaks from the fracture site); and retroauricular ecchymosis known as "Battle's sign" (bruising over the mastoid process).

Traumatic brain injury (TBI, physical trauma to the brain) can cause a variety of complications, health effects that are not TBI themselves but that result from it. The risk of complications increases with the severity of the trauma; however even mild traumatic brain injury can result in disabilities that interfere with social interactions, employment, and everyday living. TBI can cause a variety of problems including physical, cognitive, emotional, and behavioral complications.

Symptoms that may occur after a concussion – a minor form of traumatic brain injury – are referred to as post-concussion syndrome.

A basilar skull fracture is a break of a bone in the base of the skull. Symptoms may include bruising behind the ears, bruising around the eyes, or blood behind the ear drum. A cerebrospinal fluid (CSF) leak occurs in about 20% of cases and can result in fluid leaking from the nose or ear. Meningitis is a complication in about 14% of cases. Other complications include cranial nerve or blood vessel injury.

They typically require a significant degree of trauma to occur. The break is of at least one of the following bones: temporal bone, occipital bone, sphenoid bone, frontal bone, or ethmoid bone. They are divided into anterior fossa, middle fossa, and poterior fossa fractures. Facial fractures often also occur. Diagnosis is typically by CT scan.

Treatment is generally based on the injury to structures inside the head. Surgery may be done for a CSF leak that does not stop or an injury to a blood vessel or nerve. Preventative antibiotics are of unclear use. It occurs in about 12% of people with a severe head injury.

Acute injury to the internal carotid artery (carotid dissection, occlusion, pseudoaneurysm formation) may be asymptomatic or result in life-threatening bleeding. They are almost exclusively observed when the carotid canal is fractured, although only a minority of carotid canal fractures result in vascular injury. Involvement of the petrous segment of the carotid canal is associated with a relatively high incidence of carotid injury.

Symptoms of subdural hemorrhage have a slower onset than those of epidural hemorrhages because the lower pressure veins bleed more slowly than arteries. Therefore, signs and symptoms may show up in minutes, if not immediately but can be delayed as much as 2 weeks. If the bleeds are large enough to put pressure on the brain, signs of increased ICP (intracranial pressure) or damage to part of the brain will be present.

Other signs and symptoms of subdural hematoma can include any combination of the following:

- A history of recent head injury

- Loss of consciousness or fluctuating levels of consciousness

- Irritability

- Seizures

- Pain

- Numbness

- Headache (either constant or fluctuating)

- Dizziness

- Disorientation

- Amnesia

- Weakness or lethargy

- Nausea or vomiting

- Loss of appetite

- Personality changes

- Inability to speak or slurred speech

- Ataxia, or difficulty walking

- Loss of muscle control

- Altered breathing patterns

- Hearing loss or hearing ringing (tinnitus)

- Blurred Vision

- Deviated gaze, or abnormal movement of the eyes.

Subdural hematomas are divided into acute, subacute, and chronic, depending on the speed of their onset. Acute subdural hematomas that are 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.

Acute bleeds often develop after high speed acceleration or deceleration injuries and are increasingly severe with larger hematomas. 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 typically arterial bleeding of an epidural hemorrhage. Acute subdural bleeds have a high mortality rate, higher even than epidural hematomas and diffuse brain injuries, because the force (acceleration/deceleration) required to cause them causes other severe injuries as well. The mortality rate associated with acute subdural hematoma is around 60 to 80%.

Chronic subdural bleeds develop over a period of days to weeks, often after minor head trauma, though such a cause is not identifiable in 50% of patients. They may not be discovered until they present clinically months or years after a head injury. The bleeding from a chronic bleed is slow, probably from repeated minor bleeds, and usually stops by itself. Since these bleeds progress slowly, they present the chance of being stopped before they cause significant damage. Small chronic subdural hematomas, those less than a centimeter wide, have much better outcomes than acute subdural bleeds: in one study, only 22% of patients with chronic subdural bleeds had outcomes worse than "good" or "complete recovery". Chronic subdural hematomas are common in the elderly.

Intracranial hemorrhage (ICH), also known as intracranial bleed, is bleeding within the skull. It includes intracerebral bleeds (intraventricular bleeds and intraparenchymal bleeds), subarachnoid bleeds, epidural bleeds, and subdural bleeds.

Intracerebral bleeding affects 2.5 per 10,000 people each year.

The majority of blast-related ocular injuries occur in soldiers who present with other life-threatening injuries that require immediate intervention. Current Combat Support Hospital (CSH) protocol requires the surgical stabilization of any life-threatening injuries, as well as hemodynamic stability, prior to initial eye evaluation and surgical repair. Therefore, initiation of emergency ophthalmic care often occurs hours after injury. Initial examination by a military ophthalmologist begins with gross examination of each eye and orbital. 73-82% of all ocular injuries resulting from mine explosions are due to fragmentation of shrapnel upon detonation, so gross anatomical inspection by penlight may not rule out open globe injury. Harlan JB, Pieramici DJ. Evaluation of patients with ocular trauma. Ophthalmol Clin North Am. 2002; 15(2):153-61./ref> Computerized tomography (CT) may detect foreign matter and aid the clinician in determining the presence of an open-globe injury.

Epidural hematoma (EDH) is a rapidly accumulating hematoma between the dura mater and the cranium. These patients have a history of head trauma with loss of consciousness, then a lucid period, followed by loss of consciousness. Clinical onset occurs over minutes to hours. Many of these injuries are associated with lacerations of the middle meningeal artery. A "lenticular", or convex, lens-shaped extracerebral hemorrhage that does not cross suture lines will likely be visible on a CT scan of the head. Although death is a potential complication, the prognosis is good when this injury is recognized and treated.

Blast-related ocular trauma comprises a specialized group of penetrating and blunt force injuries to the eye and its structure caused by the detonation of explosive materials. The incidence of ocular trauma due to blast forces has increased dramatically with the introduction of new explosives technology into modern warfare. The availability of these volatile materials, coupled with the tactics of contemporary terrorism, has caused a rise in the number of homemade bombs capable of extreme physical harm.

Patients with intraparenchymal bleeds have symptoms that correspond to the functions controlled by the area of the brain that is damaged by the bleed. Other symptoms include those that indicate a rise in intracranial pressure caused by a large mass putting pressure on the brain.

Intracerebral hemorrhages are often misdiagnosed as subarachnoid hemorrhages due to the similarity in symptoms and signs. A severe headache followed by vomiting is one of the more common symptoms of intracerebral hemorrhage. Another common symptom is a patient can collapse. Some people may experience continuous bleeding from the ear. Some patients may also go into a coma before the bleed is noticed.

Most people who develop SCSFLS feel the sudden onset of a severe and acute headache. It is a headache usually made worse by standing, typically becoming prominent throughout the day, with the pain becoming less severe when lying down. Orthostatic headaches can become chronic and disabling to the point of incapacitation. Some patients with SCSFLS will develop headaches that begin in the afternoon. This is known as "second-half-of-the-day headache". This may be an initial presentation of a spontaneous CSF leak or appear after treatment such as an epidural patch, and likely indicates a slow CSF leak.

Apart from headache, about 50% of patients experience neck pain or stiffness, nausea, and vomiting. Other symptoms include dizziness and vertigo, facial numbness or weakness, unusually blurry or double vision, neuralgia, fatigue, or a metallic taste in the mouth. Leaking CSF can sometimes be felt or observed as a discharge from the nose or ear.

Lack of CSF pressure and volume can allow the brain to sag and descend through the foramen magnum (large opening) of the occipital bone, at the base of the skull. The lower portion of the brain is believed to stretch or impact one or more cranial nerve complexes, thereby causing a variety of sensory symptoms. Nerves that can be affected and their related symptoms are detailed in the table at right.

By far, the two most common symptoms described are pain and the feeling that teeth no longer correctly meet (traumatic malocclusion, or disocclusion). The teeth are very sensitive to pressure (proprioception), so even a small change in the location of the teeth will generate this sensation. People will also be very sensitive to touching the area of the jaw that is broken, or in the case of condylar fracture the area just in front of the tragus of the ear.

Other symptoms may include loose teeth (teeth on either side of the fracture will feel loose because the fracture is mobile), numbness (because the inferior alveolar nerve runs along the jaw and can be compressed by a fracture) and trismus (difficulty opening the mouth).

Outside the mouth, signs of swelling, bruising and deformity can all be seen. Condylar fractures are deep, so it is rare to see significant swelling although, the trauma can cause fracture of the bone on the anterior aspect of the external auditory meatus so bruising or bleeding can sometimes be seen in the ear canal. Mouth opening can be diminished (less than 3 cm). There can be numbness or altered sensation (anesthesia/paraesthesia in the chin and lower lip (the distribution of the mental nerve).

Intraorally, if the fracture occurs in the tooth bearing area, a step may seen between the teeth on either side of the fracture or a space can be seen (often mistaken for a lost tooth) and bleeding from the gingiva in the area. There can be an open bite where the lower teeth, no longer meet the upper teeth. In the case of a unilateral condylar fracture the back teeth on the side of the fracture will meet and the open bite will get progressively greater towards the other side of the mouth.

Sometimes bruising will develop in the floor of the mouth (sublingual eccymosis) and the fracture can be moved by moving either side of the fracture segment up and down. For fractures that occur in the non-tooth bearing area (condyle, ramus, and sometimes the angle) an open bite is an important clinical feature since little else, other than swelling, may be apparent.

This type of fractured mandible can involve one condyle (unilateral) or both (bilateral). Unilateral condylar fracture may cause restricted and painful jaw movement. There may be swelling over the temporomandibular joint region and bleeding from the ear because of lacerations to the external auditory meatus. The hematoma may spread downwards and backwards behind the ear, which may be confused with Battle's sign (a sign of a base of skull fracture), although this is an uncommon finding so if present, intra-cranial injury must be ruled out. If the bones fracture and overlie each other there may be shortening of the height of the ramus. This results in gagging of the teeth on the fractured side (the teeth meet too soon on the fractured side, and not on the non fractured side, i.e. "open bite" that becomes progressively worse to the unaffected side). When the mouth is opened, there may be deviation of the mandible towards the fractured side. Bilateral condylar fractures may cause the above signs and symptoms, but on both sides. Malocclusion and restricted jaw movement are usually more severe. Bilateral body or parasymphysis fractures are sometimes termed "flail mandible", and can cause involuntary posterior movement of the tongue with subsequent obstruction of the upper airway. Displacement of the condyle through the roof of glenoid fossa and into the middle cranial fossa is rare. Bilateral condylar fractures combined with a symphyseal fracture is sometimes termed a guardsman's fracture. The name comes from this injury occurring in soldiers who faint on parade grounds and strike the floor with their chin.

SCSFLS is classified into two main types, cranial leaks and spinal leaks. The vast majority of leaks are spinal. Cranial leaks occur in the head. In some of these cases, CSF can be seen dripping out of the nose, or ear. Spinal leaks occur when one or more holes form in the dura along the spinal cord. Both cranial and spinal spontaneous CSF leaks cause neurological symptoms as well as spontaneous intracranial hypotension, diminished volume and pressure of the cranium. While referred to as "intracranial hypotension", the intracranial pressure may be normal, with the underlying issue instead being low-volume CSF. For this reason SCSFLS is referred to as "CSF hypovolemia" as opposed to "CSF hypotension".

Intracerebral hemorrhage (ICH), also known as cerebral bleed, is a type of intracranial bleed that occurs within the brain tissue or ventricles. Symptoms can include headache, one-sided weakness, vomiting, seizures, decreased level of consciousness, and neck stiffness. Often symptoms get worse over time. Fever is also common. In many cases bleeding is present in both the brain tissue and the ventricles.

Causes include brain trauma, aneurysms, arteriovenous malformations, and brain tumors. The largest risk factors for spontaneous bleeding are high blood pressure and amyloidosis. Other risk factors include alcoholism, low cholesterol, blood thinners, and cocaine use. Diagnosis is typically by CT scan. Other conditions that may present similarly include ischemic stroke.

Treatment should typically be carried out in an intensive care unit. Guidelines recommended decreasing the blood pressure to a systolic of less than 140 mmHg. Blood thinners should be reversed if possible and blood sugar kept in the normal range. Surgery to place a ventricular drain may be used to treat hydrocephalus but corticosteroids should not be used. Surgery to remove the blood is useful in certain cases.

Cerebral bleeding affects about 2.5 per 10,000 people each year. It occurs more often in males and older people. About 44% of those affected die within a month. A good outcome occurs in about 20% of those affected. Strokes were first divided into their two major types, bleeding and insufficient blood flow, in 1823.

Clinical manifestations of intraparenchymal hemorrhage are determined by the size and location of hemorrhage, but may include the following:

- Hypertension, fever, or cardiac arrhythmias

- Nuchal rigidity

- Subhyaloid retinal hemorrhages

- Altered level of consciousness

- Anisocoria, Nystagmus

- Focal neurological deficits

- Putamen - Contralateral hemiparesis, contralateral sensory loss, contralateral conjugate gaze paresis, homonymous hemianopsia, aphasia, neglect, or apraxia

- Thalamus - Contralateral sensory loss, contralateral hemiparesis, gaze paresis, homonymous hemianopia, miosis, aphasia, or confusion

- Lobar - Contralateral hemiparesis or sensory loss, contralateral conjugate gaze paresis, homonymous hemianopia, abulia, aphasia, neglect, or apraxia

- Caudate nucleus - Contralateral hemiparesis, contralateral conjugate gaze paresis, or confusion

- Brain stem - Tetraparesis, facial weakness, decreased level of consciousness, gaze paresis, ocular bobbing, miosis, or autonomic instability

- Cerebellum - Ataxia, usually beginning in the trunk, ipsilateral facial weakness, ipsilateral sensory loss, gaze paresis, skew deviation, miosis, or decreased level of consciousness

Intraparenchymal hemorrhage (IPH) is one form of intracerebral bleeding in which there is bleeding within brain parenchyma. The other form is intraventricular hemorrhage (IVH).

Intraparenchymal hemorrhage accounts for approx. 8-13% of all strokes and results from a wide spectrum of disorders. It is more likely to result in death or major disability than ischemic stroke or subarachnoid hemorrhage, and therefore constitutes an immediate medical emergency. Intracerebral hemorrhages and accompanying edema may disrupt or compress adjacent brain tissue, leading to neurological dysfunction. Substantial displacement of brain parenchyma may cause elevation of intracranial pressure (ICP) and potentially fatal herniation syndromes.

Patients with arachnoid cysts may never show symptoms, even in some cases where the cyst is large. Therefore, while the presence of symptoms may provoke further clinical investigation, symptoms independent of further data cannot—and should not—be interpreted as evidence of a cyst's existence, size, location, or potential functional impact on the patient.

Symptoms vary by the size and location of the cyst(s), though small cysts usually have no symptoms and are discovered only incidentally. On the other hand, a number of symptoms may result from large cysts:

- Cranial deformation or macrocephaly (enlargement of the head), particularly in children

- Cysts in the suprasellar region in children have presented as bobbing and nodding of the head called bobble-head doll syndrome.

- Cysts in the left middle cranial fossa have been associated with ADHD in a study on affected children.

- Headaches. A patient experiencing a headache does not necessarily have an arachnoid cyst.

- In a 2002 study involving 78 patients with a migraine or tension-type headache, CT scans showed abnormalities in over a third of the patients, though arachnoid cysts only accounted for 2.6% of patients in this study.

- A study found 18% of patients with intracranial arachnoid cysts had non-specific headaches. The cyst was in the temporal location in 75% of these cases.

- Seizures

- Hydrocephalus (excessive accumulation of cerebrospinal fluid)

- Increased intracranial pressure

- Developmental delay

- Behavioral changes

- Nausea

- Hemiparesis (weakness or paralysis on one side of the body)

- Ataxia (lack of muscle control)

- Musical hallucination

- Pre-senile dementia, a condition often associated with Alzheimer's disease

- In elderly patients (>80 years old) symptoms were similar to chronic subdural hematoma or normal pressure hydrocephalus:

- Dementia

- Urinary incontinence

- Hemiparesis

- Headache

- Seizures