The bilateral form of FCMS ("also known as facio-labio-pharyngo-glosso-laryngo-brachial paralysis)" is consistent with the classic presentation of bilateral corticobulbar involvement. It is characterized by well-preserved automatic and reflex movements. It is caused by lesions in the cortical or subcortical region of the anterior opercular area surrounding the insula forming the gyri of the frontal, temporal, and parietal lobes.

The unilateral operculum syndrome is a very rare form of FCMS caused by the formation of unilateral lesions. In this form of FCMS, the unaffected hemisphere of the brain compensates for the unilateral lesion. Usually, this occurs when the unaffected region is the individual's dominant hemisphere.

Akinetic mutism can also occur as a result of damage to the mesencephalic region of the brain. Mesencephalic akinetic mutism is clinically categorized as somnolent or apathetic akinetic mutism. It is characterized by vertical gaze palsy and ophthalmoplegia. This state of akinetic mutism varies in intensity, but it is distinguished by drowsiness, lack of motivation, hyper-somnolence, and reduction in spontaneous verbal and motor actions.

Akinetic mutism can occur in the frontal region of the brain and occurs because of bilateral frontal lobe damage. Akinetic mutism as a result of frontal lobe damage is clinically characterized as hyperpathic. It occurs in patients with bilateral circulatory disturbances in the supply area of the anterior cerebral artery.

Anosodiaphoria is a condition in which a person who suffers disability due to brain injury seems indifferent to the existence of their handicap. Anosodiaphoria is specifically used in association with indifference to paralysis. It is a somatosensory agnosia, or a sign of neglect syndrome. It might be specifically associated with defective functioning of the frontal lobe of the right hemisphere.

Joseph Babinski first used the term anosodiaphoria in 1914 to describe a disorder of the body schema in which patients verbally acknowledge a clinical problem (such as hemiparesis) but fail to be concerned about it. Anosodiaphoria follows a stage of anosognosia, in which there may be verbal, explicit denial of the illness, and after several days to weeks, develop the lack of emotional response. Indifference is different from denial because it implies a lack of caring on the part of the patient whom otherwise acknowledges his or her deficit.

The cardinal features of Rolandic epilepsy are infrequent, often single, focal seizures consisting of:

Hemifacial sensorimotor seizures are often entirely localised in the lower lip or spread to the ipsilateral hand. Motor manifestations are sudden, continuous or bursts of clonic contractions, usually lasting from a few seconds to a minute. Ipsilateral tonic deviation of the mouth is also common. Hemifacial sensory symptoms consist of unilateral numbness mainly in the corner of the mouth.

Hemifacial seizures are often associated with an inability to speak and hypersalivation:

"The left side of my mouth felt numb and started jerking and pulling to the left, and I could not speak to say what was happening to me."

Negative myoclonus can be observed in some cases, as an interruption of tonic muscular activity

Oropharyngolaryngeal ictal manifestations are unilateral sensorimotor symptoms inside the mouth. Numbness, and more commonly paraesthesias (tingling, prickling, freezing), are usually diffuse on one side or, exceptionally, may be highly localised even to one tooth. Motor oropharyngolaryngeal symptoms produce strange sounds, such as death rattle, gargling, grunting and guttural sounds, and combinations:

"In his sleep, he was making guttural noises, with his mouth pulled to the right, ‘as if he was chewing his tongue’". "We heard her making strange noises ‘like roaring’ and found her unresponsive, head raised from the pillow, eyes wide open, rivers of saliva coming out of her mouth, rigid."

Arrest of speech is a form of anarthria. The child is unable to utter a single intelligible word and attempts to communicate with gestures.

"My mouth opened and I could not speak. I wanted to say I cannot speak. At the same time, it was as if somebody was strangling me."

Hypersalivation , a prominent autonomic manifestation, is often associated with hemifacial seizures, oro-pharyngo-laryngeal symptoms and speech arrest. Hypersalivation is not just frothing:

"Suddenly my mouth is full of saliva, it runs out like a river and I cannot speak."

Syncope-like epileptic seizures may occur, probably as a concurrent symptom of Panayiotopoulos syndrome:

"She lies there, unconscious with no movements, no convulsions, like a wax work, no life."

Consciousness and recollection are fully retained in more than half (58%) of Rolandic seizures.

"I felt that air was forced into my mouth, I could not speak and I could not close my mouth. I could understand well everything said to me. Other times I feel that there is food in my mouth and there is also a lot of salivation. I cannot speak."

In the remainder (42%), consciousness becomes impaired during the ictal progress and in one third there is no recollection of ictal events.

Progression to hemiconvulsions or generalised tonic–clonic seizures occurs in around half of children and hemiconvulsions may be followed by postictal Todd’s hemiparesis .

Duration and circadian distribution: Rolandic seizures are usually brief, lasting for 1–3 min. Three quarters of seizures occur during nonrapid eye movement sleep, mainly at sleep onset or just before awakening.

Status epilepticus: Although rare, focal motor status or hemiconvulsive status epilepticus is more likely to occur than secondarily generalised convulsive status epilepticus, which is exceptional. Opercular status epilepticus usually occurs in children with atypical evolution or may be induced by carbamazepine or lamotrigine. This state lasts for hours to months and consists of ongoing unilateral or bilateral contractions of the mouth, tongue or eyelids, positive or negative subtle perioral or other myoclonus, dysarthria, speech arrest, difficulties in swallowing, buccofacial apraxia and hypersalivation. These are often associated with continuous spikes and waves on an EEG during NREM sleep.

Other seizure types: Despite prominent hypersalivation, focal seizures with primarily autonomic manifestations (autonomic seizures) are not considered part of the core clinical syndrome of Rolandic epilepsy. However, some children may present with independent autonomic seizures or seizures with mixed Rolandic-autonomic manifestations including emesis as in Panayiotopoulos syndrome.

Atypical forms: Rolandic epilepsy may present with atypical manifestations such early age at onset, developmental delay or learning difficulties at inclusion, other seizure types, atypical EEG abnormalities.

These children usually have normal intelligence and development. Learning can remain unimpaired while a child is afflicted with Rolandic epilepsy.

Benign Rolandic epilepsy or benign childhood epilepsy with centrotemporal spikes (BCECTS) is the most common epilepsy syndrome in childhood. Most children will outgrow the syndrome (it starts around the age of 3-13 with a peak around 8–9 years and stops around age 14-18), hence the label benign. The seizures, sometimes referred to as "sylvian seizures", start around the central sulcus of the brain (also called the centrotemporal area, located around the Rolandic fissure, after Luigi Rolando).

A few possible explanations for anosodiaphoria exist:

1. The patient is aware of the deficit but does not fully comprehend it or its significance for functioning

2. May be related to an affective communication disorder and defective arousal. These emotional disorders cannot account for the verbal explicit denial of illness of anosognosia.

Other explanations include reduced emotional experience, impaired emotional communication, alexithymia, behavioral abnormalities, dysexecutive syndrome, and the frontal lobes.

Partial Anterior Circulation Infarct (PACI) is a type of cerebral infarction affecting part of the anterior circulation supplying one side of the brain.

Partial Anterior Circulation Stroke Syndrome (PACS) refers to the symptoms of a patient who clinically appears to have suffered from a partial anterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It is diagnosed by any one of the following

- 2 out of 3 features of

- Higher dysfunction

- Dysphasia

- Visuospatial disturbances

- Homonymous hemianopia

- Motor and Sensory Defects (>2/3 of face, arm, leg)

- Higher dysfunction alone

- Partial Motor or Sensory Defect

If all of the above symptoms are present, a Total Anterior Circulation Infarct is more likely.

For more information, see stroke.

Aboulia has been known to clinicians since 1838. However, in the time since its inception, the definition of aboulia has been subjected to many different forms, some contradictory. Aboulia has been described as a loss of drive, expression, loss of behavior and speech output, slowing and prolonged speech latency, and reduction of spontaneous thought content and initiative. The clinical features most commonly associated with aboulia are:

- Difficulty in initiating and sustaining purposeful movements

- Lack of spontaneous movement

- Reduced spontaneous speech

- Increased response-time to queries

- Passivity

- Reduced emotional responsiveness and spontaneity

- Reduced social interactions

- Reduced interest in usual pastimes

Especially in patients with progressive dementia, it may affect feeding. Patients may continue to chew or hold food in their mouths for hours without swallowing it. The behavior may be most evident after these patients have eaten part of their meals and no longer have strong appetites.

A Total Anterior Circulation Infarct (TACI) is a type of cerebral infarction affecting the entire anterior circulation supplying one side of the brain.

Total Anterior Circulation Stroke Syndrome (TACS) refers to the symptoms of a patient who clinically appears to have suffered from a total anterior circulation infarct, but who has not yet had any diagnostic imaging (e.g. CT Scan) to confirm the diagnosis.

It is diagnosed when it causes all 3 of the following symptoms:

- Higher dysfunction

- Dysphasia

- Visuospatial disturbances

- Decreased level of consciousness

- Homonymous hemianopia

- Motor and Sensory Defects (≥2/3 of face, arm, leg)

For more information, see stroke.

Aboulia or abulia (from , meaning "will", with the prefix -a), in neurology, refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM). Aboulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than aboulia. A patient with aboulia is unable to act or make decisions independently. It may range in severity from subtle to overwhelming. It is also known as Blocq's disease (which also refers to abasia and astasia-abasia). Aboulia was originally considered to be a disorder of the will.

The condition usually consists of:

Sensation to the face is preserved, due to the sparing of the trigeminal nucleus.

The syndrome is said to be "alternating" because the lesion causes symptoms both contralaterally and ipsilaterally. Sensation of pain and temperature is preserved, because the spinothalamic tract is located more laterally in the brainstem and is also not supplied by the anterior spinal artery (instead supplied by the posterior inferior cerebellar arteries and the vertebral arteries).

Changes in muscle performance can be broadly described as the upper motor neuron syndrome. These changes vary depending on the site and the extent of the lesion, and may include:

- Muscle weakness. A pattern of weakness in the extensors (upper limbs) or flexors (lower limbs), is known as 'pyramidal weakness'

- Decreased control of active movement, particularly slowness

- Spasticity, a velocity-dependent change in muscle tone

- Clasp-knife response where initial higher resistance to movement is followed by a lesser resistance

- Babinski sign is present, where the big toe is raised (extended) rather than curled downwards (flexed) upon appropriate stimulation of the sole of the foot. The presence of the Babinski sign is an abnormal response in adulthood. Normally, during the plantar reflex, it causes plantar flexion and the adduction of the toes. In Babinski's sign, there is dorsiflexion of the big toe and abduction of the other toes. Physiologically, it is normally present in infants from birth to 12 months. The presence of the Babinski sign after 12 months is the sign of a non-specific upper motor neuron lesion.

- Increased deep tendon reflex (DTR)

- Pronator drift

Medial medullary syndrome, also known as inferior alternating syndrome, hypoglossal alternating hemiplegia, lower alternating hemiplegia, or Dejerine syndrome, is a type of alternating hemiplegia characterized by a set of clinical features resulting from occlusion of the anterior spinal artery. This results in the infarction of medial part of the medulla oblongata.

Damage to the following areas produces symptoms (from medial to lateral):

The extensor Babinski reflex is usually absent. Muscle paresis/paralysis, hypotonia/atonia, and hyporeflexia/areflexia are usually seen immediately following an insult. Muscle wasting, fasciculations and fibrillations are typically signs of end-stage muscle denervation and are seen over a longer time period. Another feature is the segmentation of symptoms – only muscles innervated by the damaged nerves will be symptomatic.

A lateral pontine syndrome is a lesion which is similar to the lateral medullary syndrome, but because it occurs in the pons, it also involves the cranial nerve nuclei of the pons.

These are the neural tracts which descend in the ventral horn of the spinal cord, carrying signals for voluntary movement of skeletal muscle. From their origin in the primary motor cortex, these nerves pass via the corona radiata to gather in the internal capsule before crossing over to the opposite side (decussation) in the medullary pyramids and proceeding down the spinal cord to meet lower motor neurons in the anterior grey column.

Most common causes of lower motor neuron injuries are trauma to peripheral nerves that serve the axons – a virus that selectively attacks ventral horn cells.

Disuse atrophy of the muscle occurs i.e., shrinkage of muscle fibre finally replaced by fibrous tissue (fibrous muscle)

Other causes include Guillain–Barré syndrome, "C. botulism", polio, and cauda equina syndrome; another common cause of lower motor neuron degeneration is amyotrophic lateral sclerosis.

The most common finding is oculomotor nerve dysfunction leading to ophthalmoplegia. This is often accompanied by ophthalmic nerve dysfunction, leading to hypoesthesia of the upper face. The optic nerve may eventually be involved, with resulting visual impairment.

Orbital apex syndrome, also known as Jacod syndrome, is a collection of cranial nerve deficits associated with a mass lesion near the apex of the orbit of the eye. This syndrome is a separate entity from Rochon–Duvigneaud syndrome, which occurs due to a lesion immediately anterior to the orbital apex. Most commonly optic nerve is involved.

Worster-Drought syndrome is a form of congenital suprabulbar paresis that occurs in some children with cerebral palsy. It is caused by inadequate development of the corticobulbar tracts and causes problems with the mouth and tongue including impaired swallowing. A similar syndrome in adults is called anterior opercular syndrome.

A 1986 study of a family in which multiple members had Worster-Drought Syndrome suggested it might be hereditary.

A 2000 review of cases classified Worster-Drought Syndrome as a form of cerebral palsy, caused by early damage to the brain, but identified no obvious causes during gestation or birth and found some families with a history of the condition.

The syndrome was named after Cecil Charles Worster-Drought, the doctor who discovered it in 1956.

Anterior cerebral artery syndrome is a condition whereby the blood supply from the anterior cerebral artery (ACA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the medial aspects of the frontal and parietal lobes, basal ganglia, anterior fornix and anterior corpus callosum.

Depending upon the area and severity of the occlusion, signs and symptoms may vary within the population affected with ACA syndrome. Blockages to the proximal (A1) segment of the vessel produce only minor deficits due to the collateral blood flow from the opposite hemisphere via the anterior communicating artery. Occlusions distal to this segment will result in more severe presentation of ACA syndrome. Contralateral hemiparesis and hemisensory loss of the lower extremity is the most common symptom associated with ACA syndrome.

There are seven major symptoms of Korsakoff's syndrome (amnestic-confabulatory syndrome):

1. anterograde amnesia, memory loss for events after the onset of the syndrome

2. retrograde amnesia, memory loss extends back for some time before the onset of the syndrome

3. amnesia of fixation, also known as fixation amnesia (loss of immediate memory, a person being unable to remember events of the past few minutes)

4. confabulation, that is, invented memories which are then taken by the patient as true due to gaps in memory, with such gaps sometimes associated with blackouts

5. minimal content in conversation

6. lack of insight

7. apathy – the patients lose interest in things quickly, and generally appear indifferent to change.

Benon R. and LeHuché R. (1920) described the characteristic signs of Korsakoff syndrome with some additional features: confabulation (false memories), fixation amnesia, paragnosia or false recognition of places, mental excitation, euphoria, etc.

Thiamine is essential for the decarboxylation of pyruvate, and deficiency during this metabolic process is thought to cause damage to the medial thalamus and mammillary bodies of the posterior hypothalamus, as well as generalized cerebral atrophy. These brain regions are all parts of the limbic system, which is heavily involved in emotion and memory.

Korsakoff's involves neuronal loss, that is, damage to neurons; gliosis, which is a result of damage to supporting cells of the central nervous system, and hemorrhage or bleeding also occurs in mammillary bodies. Damage to the dorsomedial nucleus or anterior group of the thalamus (limbic-specific nuclei) is also associated with this disorder. Cortical dysfunction may have arisen from thiamine deficiency, alcohol neurotoxicity, and/or structural damage in the diencephalon.

Originally, it was thought that a lack of initiative and a flat affect were important characteristics of emotional presentation in sufferers. Studies have questioned this, proposing that neither is necessarily a symptom of Korsakoff's. Research suggesting that Korsakoff's patients are emotionally unimpaired has made this a controversial topic. It can be argued that apathy, which usually characterizes Korsakoff's patients, reflects a deficit of emotional "expressions", without affecting the "experience" or perception of emotion.

Korsakoff's Syndrome causes deficits in declarative memory in most patients, but leaves implicit spatial, verbal, and procedural memory functioning intact. People who have Korsakoff's syndrome have deficits in the processing of contextual information. Context memories refers to the where and when of experiences, and is an essential part of recollection. The ability to store and retrieve this information, such as spatial location or temporal order information, is impaired.

Research has also suggested that Korsakoff patients have impaired executive functions, which can lead to behavioral problems and interfere with daily activities. It is unclear, however, which executive functions are affected most. Nonetheless, IQ is usually not affected by the brain damage associated with Korsakoff's syndrome.

At first it was thought that Korsakoff's patients used confabulation to fill in memory gaps. However, it has been found that confabulation and amnesia do not necessarily co-occur. Studies have shown that there is dissociation between provoked confabulation, spontaneous confabulation (which is unprovoked), and false memories. That is, patients could be led to believe certain things had happened which actually had not, but so could people without Korsakoff’s syndrome.