The signs and symptoms of brain tumors are broad. People with brain tumors will experience them no matter if the tumor is benign (not cancerous) or cancerous. Primary and secondary brain tumors present with similar symptoms, depending on the location, size, and rate of growth of the tumor. For example, larger tumors in the frontal lobe can cause changes in the ability to think. However, a smaller tumor in an area such as Wernicke's area (small area responsible for language comprehension) can result in a greater loss of function.

Common symptoms include, but are not necessarily limited to:

- Lack of facial control, (droopy eyelids)

- Double vision

- Headache or headache that gets better after vomiting

- Nausea and vomiting

- Weakness and fatigue

- Seizures

- Balance problems

- Numbness in face

Symptoms can develop slowly and subtly and may go unnoticed for months. In other cases, the symptoms may arise abruptly. A sudden onset of symptoms tends to occur with more rapidly growing, high-grade tumors.

Gliomas can be classified according to whether they are above or below a membrane in the brain called the tentorium. The tentorium separates the cerebrum (above) from the cerebellum (below).

- The supratentorial is above the tentorium, in the cerebrum, and mostly found in adults (70%).

- The infratentorial is below the tentorium, in the cerebellum, and mostly found in children (70%).

- The pontine tumors are located in the pons of the brainstem. The brainstem has three parts (pons, midbrain, and medulla); the pons controls critical functions such as breathing, making surgery on these extremely dangerous.

Headaches as a result of raised intracranial pressure can be an early symptom of brain cancer. However, isolated headache without other symptoms is rarer, and other symptoms often occur before headaches become common. Certain warning signs for headache exist which make it more likely to be associated with brain cancer. These are as defined by the American Academy of Neurology: "abnormal neurological examination, headache worsened by Valsalva maneuver, headache causing awakening from sleep, new headache in the older population, progressively worsening headache, atypical headache features, or patients who do not fulfill the strict definition of migraine".

Symptoms of gliomas depend on which part of the central nervous system is affected. A brain glioma can cause headaches, vomiting, seizures, and cranial nerve disorders as a result of increased intracranial pressure. A glioma of the optic nerve can cause visual loss. Spinal cord gliomas can cause pain, weakness, or numbness in the extremities. Gliomas do not metastasize by the bloodstream, but they can spread via the cerebrospinal fluid and cause "drop metastases" to the spinal cord.

A child who has a subacute disorder of the central nervous system that produces cranial nerve abnormalities (especially of cranial nerve VII and the lower bulbar nerves), long-tract signs, unsteady gait secondary to spasticity, and some behavioral changes is most likely to have a pontine glioma.

A brainstem glioma is a cancerous glioma tumor in the brainstem. Around 75% are diagnosed in children and young adults under the age of twenty, but have been known to affect older adults as well. Brainstem gliomas start in the brain or spinal cord tissue and typically spread throughout the nervous system.

Medulloepithelioma most commonly affect children between 6 months and 5 years; rarely, this tumour may occur congenitally or beyond this age range. Incidence is equal in males and females.

Gliosarcoma is a rare type of glioma, a cancer of the brain that comes from glial, or supportive, brain cells, as opposed to the neural brain cells. Gliosarcoma is a malignant cancer, and is defined as a glioblastoma consisting of gliomatous and sarcomatous components.

It is estimated that approximately 2.1% of all glioblastomas are gliosarcomas. Although most gliomas rarely show metastases outside the cerebrum, gliosarcomas have a propensity to do so, most commonly spreading through the blood to the lungs, and also liver and lymph nodes.

Gliosarcomas have an epidemiology similar to that of glioblastomas, with the average age of onset being 54 years, and males being affected twice as often as females. They are most commonly present in the temporal lobe.

Medulloepithelioma is a rare, primitive, fast-growing brain tumour thought to stem from cells of the embryonic medullary cavity. Tumours originating in the ciliary body of the eye are referred to as embryonal medulloepitheliomas, or diktyomas.

A highly malignant undifferentiated primitive neuroepithelial tumour of children, medulloepithelioma may contain bone, cartilage, skeletal muscle, and tends to metastasize extracranially.

An MRI is better than a CT scan when a brainstem tumor is in the differential diagnosis.

The symptoms of brain stem tumors vary greatly and can include ataxia, cranial nerve palsy, headaches, problems with speech and swallowing, hearing loss, weakness, hemiparesis, vision abnormalities, ptosis, and behavioral changes. Another possible symptom is vomiting. Headaches related to brainstem tumors may be worse shortly after waking up in the morning.

Early symptoms are easily overlooked, sometimes mistaken for the normal changes of aging or attributed to noise exposure earlier in life, often delaying diagnosis. The most prevalent symptoms in patients suffering from vestibular schwannoma is hearing loss (94 %), tinnitus (83 %) and vertigo (49 %).

A vestibular schwannoma (VS) is a benign primary intracranial tumor of the myelin-forming cells of the vestibulocochlear nerve (8th cranial nerve). A type of schwannoma, this tumor arises from the Schwann cells responsible for the myelin sheath that helps keep peripheral nerves insulated. Although it is also called an acoustic neuroma, this a misnomer for two reasons. First, the tumor usually arises from the vestibular division of the vestibulocochlear nerve, rather than the cochlear division. Second, it is derived from the Schwann cells of the associated nerve, rather than the actual neurons (neuromas).

Approximately 2,000 to 3,000 cases are diagnosed each year in the United States (6 to 9 per million persons). Comprehensive studies from Denmark published in 2012 showed an annual incidence of 19-23 per million from 2002 to 2008, over the last 30 years the reported incidence have been increasing, until the last decade in which an approximation of the true incidence may have been found. Most recent publications suggest that the incidence of vestibular schwannomas have been rising because of advances in MRI scanning.

Most cases are diagnosed in people between the ages of 30 and 60, and men and women appear to be affected equally. Most vestibular schwannomas occur spontaneously in those without a family history. One confirmed risk factor is a rare genetic mutation called NF2.

The primary symptoms of vestibular schwannoma are unexplained progressive unilateral hearing loss and tinnitus, and vestibular (disequilibrium) symptoms. Treatment of the condition is by surgery or radiation, and often results in substantial or complete hearing loss in the affected ear. Observation (non-treatment) over time also usually results in hearing loss in the affected ear.

The cerebellopontine angle is the anatomic space between the cerebellum and the pons filled with cerebrospinal fluid. This is a common site for the growth of acoustic neuromas or schwannomas. A distinct neurologic syndrome of deficits occurs due to the anatomic proximity of the cerebellopontine angle to specific cranial nerves. Indications include unilateral hearing loss (85%), speech impediments, disequilibrium, tremors or other loss of motor control.

Tumors within the nerve canaliculi initially present with unilateral sensorineural hearing loss, unilateral tinnitus, or disequilibrium (vertigo is rare, on account of the slow growth of neuromas). Speech discrimination out of proportion to hearing loss, difficulty talking on the telephone are frequent accompaniments. Tumors extending into the CPA will likely present with disequilibrium or ataxia depending on the amount of extension on the brainstem. With brainstem extension, midfacial and corneal hypesthesia, hydrocephalus, and other cranial neuropathies become more prevalent.

For example, involvement of CN V from a cerebellopontine mass lesion often results in loss of the ipsilateral (same side of the body) corneal reflex (involuntary blink).

Patients with larger tumours can develop Bruns nystagmus ('dancing eyes') due to compression of the flocculi.

Brain herniation is a potentially deadly side effect of very high pressure within the skull that occurs when a part of the brain is squeezed across structures within the skull. The brain can shift across such structures as the falx cerebri, the tentorium cerebelli, and even through the foramen magnum (the hole in the base of the skull through which the spinal cord connects with the brain). Herniation can be caused by a number of factors that cause a mass effect and increase intracranial pressure (ICP): these include traumatic brain injury, intracranial hemorrhage, or brain tumor.

Herniation can also occur in the absence of high ICP when mass lesions such as hematomas occur at the borders of brain compartments. In such cases local pressure is increased at the place where the herniation occurs, but this pressure is not transmitted to the rest of the brain, and therefore does not register as an increase in ICP.

Because herniation puts extreme pressure on parts of the brain and thereby cuts off the blood supply to various parts of the brain, it is often fatal. Therefore, extreme measures are taken in hospital settings to prevent the condition by reducing intracranial pressure, or decompressing (draining) a hematoma which is putting local pressure on a part of the brain.

Cerebellar stroke syndrome is a condition in which the circulation to the cerebellum is impaired due to a lesion of the superior cerebellar artery, anterior inferior cerebellar artery or the posterior inferior cerebellar artery.

Cardinal signs include vertigo, headache, vomiting, and ataxia.

Cerebellar strokes account for only 2-3% of the 600 000 strokes that occur each year in the United States. They are far less common than strokes which occur in the cerebral hemispheres. In recent years mortality rates have decreased due to advancements in health care which include earlier diagnosis through MRI and CT scanning. Advancements have also been made which allow earlier management for common complications of cerebellar stroke such as brainstem compression and hydrocephalus.

Research is still needed in the area of cerebellar stroke management; however, it has been proposed that several factors may lead to poor outcomes in individuals who suffer from cerebellar stroke. These factors include:

1. Declining levels of consciousness

2. New signs of brainstem involvement

3. Progressing Hydrocephalus

4. Stroke to the midline of the cerebellum (a.k.a. the vermis)

Brain herniation frequently presents with abnormal posturing a characteristic positioning of the limbs indicative of severe brain damage. These patients have a lowered level of consciousness, with Glasgow Coma Scores of three to five. One or both pupils may be dilated and fail to constrict in response to light. Vomiting can also occur due to compression of the vomiting center in the medulla oblongata.

Movement Disorder

- Dystonia

- Parkinsonism

- Chorea

- Ocular flutter

- Motor tics

Psychiatric Symptoms

- Agitation

- Emotional lability

- Psychosis

- Depression

Associated symptoms

- Encephalopathy

- Sleep disorder

- Reduced consciousness

- Mutism

Within a few days, usually less than 2 weeks patients develop

- Behavioral disturbance: agitation

- Auditory and visual hallucinations,

- Delusions

- Psychosis

- Amnesia,

- Seizures,

- Dyskinesias, Catatonia, orolingual dyskinesias and stereotypic movement

- Autonomic dysfunction, and

- Decreased level of consciousness often requiring ventilatory support.

The blockage of cerebrospinal fluid (CSF) flow may also cause a syrinx to form, eventually leading to syringomyelia. Central cord symptoms such as hand weakness, dissociated sensory loss, and, in severe cases, paralysis may occur.

Chiari malformations (CMs) are structural defects in the cerebellum. They consist of a downward displacement of the cerebellar tonsils through the foramen magnum (the opening at the base of the skull), sometimes causing non-communicating hydrocephalus as a result of obstruction of cerebrospinal fluid (CSF) outflow. The cerebrospinal fluid outflow is caused by phase difference in outflow and influx of blood in the vasculature of the brain. The malformation is named for Austrian pathologist Hans Chiari. A type II CM is also known as an Arnold–Chiari malformation in honor of Chiari and German pathologist Julius Arnold.

CMs can cause headaches, difficulty swallowing (sometimes accompanied by gagging), choking and vomiting, dizziness, nausea, neck pain, unsteady gait (problems with balance), poor hand coordination (fine motor skills), numbness and tingling of the hands and feet, and speech problems (such as hoarseness).

Less often, people with Chiari malformation may experience ringing or buzzing in the ears (tinnitus), weakness, slow heart rhythm, or fast heart rhythm, curvature of the spine (scoliosis) related to spinal cord impairment, abnormal breathing, such as central sleep apnea, characterized by periods of breathing cessation during sleep, and, in severe cases, paralysis.

Typical symptoms of PRES, listed according to prevalence, include: altered mental status (encephalopathy), seizure, and headache. Less commonly there may be visual disturbances, focal neurologic signs, and status epilepticus.

Symptoms can develop over several weeks to months. Symptoms depend on location of damage in the brain and the degree of damage. The most prominent symptoms are "clumsiness, progressive weakness and visual, speech, and sometimes personality changes"

The lesions affecting the parietal and occipital lobes can lead to a phenomenon known as alien hand syndrome.

Clinical presentation of CPM is heterogeneous and depend on the regions of the brain involved. Prior to its onset, patients may present with the neurological signs and symptoms of hyponatraemic encephalopathy such as nausea and vomiting, confusion, headache and seizures. These symptoms may resolve with normalisation of the serum sodium concentration. Three to five days later, a second phase of neurological manifestations occurs correlating with the onset of myelinolysis. Observable immediate precursors may include seizures, disturbed consciousness, gait changes, and decrease or cessation of respiratory function.

The classical clinical presentation is the progressive development of spastic quadriparesis, pseudobulbar palsy, and emotional lability (pseudobulbar affect), with other more variable neurological features associated with brainstem damage. These result from a rapid myelinolysis of the corticobulbar and corticospinal tracts in the brainstem.