Weber's syndrome (also known as superior alternating hemiplegia) has a few distinct symptoms: contralateral hemiparesis of limb and facial muscle accompanied by weakness in one or more muscles that control eye movement on the same side. Another symptom that appears is the loss of eye movement due to damage to the oculomotor nerve fibers. The upper and lower extremities have increased weakness.

Middle alternating hemiplegia typically constitutes weakness of the extremities accompanied by paralysis of the extraocular muscle specifically lateral rectus, on the opposite side of the affected extremities, which indicates a lesion in the caudal and medial pons involving the abducens nerve root (controls movement of the eye) and corticospinal fibers (carries motor commands from the brain to the spinal cord).

People with hemiparesis often have difficulties maintaining their balance due to limb weaknesses leading to an inability to properly shift body weight. This makes performing everyday activities such as dressing, eating, grabbing objects, or using the bathroom more difficult. Hemiparesis with origin in the lower section of the brain creates a condition known as ataxia, a loss of both gross and fine motor skills, often manifesting as staggering and stumbling. Pure Motor Hemiparesis, a form of hemiparesis characterized by sided weakness in the leg, arm, and face, is the most commonly diagnosed form of hemiparesis.

Individuals who present with pusher syndrome or lateropulsion, as defined by Davies, vary in their degree and severity of this condition and therefore appropriate measures need to be implemented in order to evaluate the level of "pushing". There has been a shift towards early diagnosis and evaluation of functional status for individuals who have suffered from a stroke and presenting with pusher syndrome in order to decrease the time spent as an in-patient at hospitals and promote the return to function as early as possible. Moreover, in order to assist therapists in the classification of pusher syndrome, specific scales have been developed with validity that coincides with the criteria set out by Davies’ definition of "pusher syndrome". In a study by Babyar "et al.", an examination of such scales helped determine the relevance, practical aspects and clinimetric properties of three specific scales existing today for lateropulsion. The three scales examined were the Clinical Scale of Contraversive Pushing, Modified Scale of Contraversive Pushing, and the Burke Lateropulsion Scale. The results of the study show that reliability for each scale is good; moreover, the Scale of Contraversive Pushing was determined to have acceptable clinimetric properties, and the other two scales addressed more functional positions that will help therapists with clinical decisions and research.

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).

Spastic hemiplegia is a neuromuscular condition of spasticity that results in the muscles on one side of the body being in a constant state of contraction. It is the "one-sided version" of spastic diplegia. It falls under the mobility impairment umbrella of cerebral palsy. About 20–30% of people with cerebral palsy have spastic hemiplegia. Due to brain or nerve damage, the brain is constantly sending action potentials to the neuromuscular junctions on the affected side of the body. Similar to strokes, damage on the left side of the brain affects the right side of the body and damage on the right side of the brain affects the left side of the body.

The affected side of the body is rigid, weak and has low functional abilities. In most cases, the upper extremity is much more affected than the lower extremity. This could be due to preference of hand usage during early development. If both arms are affected, the condition is referred to as double hemiplegia. Some patients with spastic hemiplegia only suffer minor impairments, where in severe cases one side of the body could be completely paralyzed. The severity of spastic hemiplegia is dependent upon the degree of the brain or nerve damage.

FHM signs overlap significantly with those of migraine with aura. In short, FHM is typified by migraine with aura associated with hemiparesis and, in FHM1, cerebellar degeneration. This cerebellar degeneration can result in episodic or progressive ataxia. FHM can also present with the same signs as benign familial infantile convulsions (BFIC) and alternating hemiplegia of childhood. Other symptoms are altered consciousness (in fact, some cases seem related to head trauma), gaze-evoked nystagmus and coma. Aura symptoms, such as numbness and blurring of vision, typically persist for 30–60 minutes, but can last for weeks and months. An attack resembles a stroke, but unlike a stroke, it resolves in time. These signs typically first manifest themselves in the first or second decade of life.

AHC patients exhibit a wide range of symptoms in addition to hemiplegic attacks. These can be further characterized as paroxysmal and non-paroxysmal symptoms. Paroxysmal symptoms are generally associated with hemiplegic attacks and may occur suddenly with hemiplegia or on their own. Paroxysmal symptoms may last for variable amounts of time. Non-paroxysmal symptoms tend to be side effects of AHC which are present at all times, not just during episodes or attacks. Epilepsy, which is also considered a paroxysmal symptom, plays an important role in the progression and diagnosis of AHC.

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.

Chronologically, hemiplegic attacks are not always the first symptom of AHC, but they are the most prominent symptom, as well as the symptom for which the disorder is named. Hemiplegic attacks may affect one or both sides of the body, and attacks which affect both sides of the body may be referred to as either or quadriplegic attacks. One of the unique characteristics of AHC is that hemiplegic attacks, as well as other symptoms which may co-occur with hemiplegia, cease immediately upon sleep. During strong attacks, the symptoms may reoccur upon waking. Hemiplegic attacks can occur suddenly or gradually, and the severity of an attack can vary over its duration. The attacks may alternate from one side of the body to another, though this is rare. The length of attacks may also vary from minutes to weeks, though length of attacks varies more greatly between people than between attacks for one person. Both bilateral and hemiplegic attacks are associated with pseudobulbar features such as dysphagia, dysarthria, and respiratory difficulty. Paralysis is also often accompanied by changes in skin color and temperature, sweating, restlessness, tremor, screaming, and the appearance of pain. Hemiplegic attacks happen irregularly and can occur with speech, eating, and swallowing impairment. Patients with AHC are frequently underweight due to these side effects. The average age of onset for hemiplegic episodes has been found to be 6–7 months of age. This early onset gives the name of this disorder the slightly misleading ending 'of childhood'. AHC is not exclusively limited to childhood – attacks become milder after the first ten years of life, but they never completely disappear.

The specific and familial association of BIFE and PKC defines a novel clinical entity : the infantile convulsions and choreoathetosis syndrome. The first observation was made in four families where children were affected with nonfebrile convulsions at age 3–12 months.Partial epileptic seizures started with a psychomotor arrest and a deviation of the head and eyes to one side, followed inconstantly by unilateral jerks.In some cases, seizures generalized secondarily. None of the interictal electroencephalograms showed epileptiform abnormalities, and magnetic-resonance imaging were normal. These convulsions had a favorable outcome. At 5–8 years of age affected children developed abnormal movements. They presented with twisting movements of the hands of a reptilian type when stressed or embarrassed. They also developed jerky movements of the legs after running. Initially, abnormal movements were intermediate in speed between quick and slow, typical of paroxysmal choreoathetosis. Combinations of abnormal movements involving the arms, legs, trunk and occasionally the head were observed. The attacks lasted only a few minutes, occurring with a frequency of 5-30 episodes per day and were not accompanied by unconsciousness. In all patients, abnormal movements disappeared at 25–30 years of age without any treatment. Since the first report similar clinical presentations have been published which confirm the specificity of the ICCA syndrome.

Benign occipital epilepsy of childhood (BOEC) is an idiopathic localization-related epilepsy and consists of an evolving group of syndromes. Most authorities include two subtypes, an early subtype with onset between three and five years, and a late onset between seven and 10 years. Seizures in BOEC usually feature visual symptoms such as scotoma or fortifications (brightly colored spots or lines) or amaurosis (blindness or impairment of vision). Convulsions involving one half the body, hemiconvulsions, or forced eye deviation or head turning are common. Younger patients typically experience symptoms similar to migraine with nausea and headache, and older patients typically complain of more visual symptoms. The EEG in BOEC shows spikes recorded from the occipital (back of head) regions. The EEG and genetic pattern suggest an autosomal dominant transmission as described by Ruben Kuzniecky, et al. Lately, a group of epilepsies termed Panayiotopoulos syndrome that share some clinical features of BOEC but have a wider variety of EEG findings are classified by some as BOEC.

Benign centrotemporal lobe epilepsy of childhood or benign Rolandic epilepsy is an idiopathic localization-related epilepsy that occurs in children between the ages of 3 and 13 years, with peak onset in prepubertal late childhood. Apart from their seizure disorder, these patients are otherwise normal. This syndrome features simple focal seizures that involve facial muscles and frequently cause drooling. Although most episodes are brief, seizures sometimes spread and generalize. Seizures are typically nocturnal and confined to sleep. The EEG may demonstrate spike discharges that occur over the centrotemporal scalp over the central sulcus of the brain (the Rolandic sulcus) that are predisposed to occur during drowsiness or light sleep. Seizures cease near puberty. Seizures may require anticonvulsant treatment, but sometimes are infrequent enough to allow physicians to defer treatment.

Spastic quadriplegia can be detected by the abnormal development of motor skills in children. Symptoms can present themselves as early as three months but are generally seen before the child reaches two years of age. Some warning signs include: a child of more than two months who has stiff legs that scissor and is unable to control his or her head, and a child of more than twelve months who has not developed the ability to crawl or stand.

Spastic quadriplegia also presents a range of symptoms that affect the musculature. Many experience contractures, which are defined as joints that cannot be stretched or moved. Clonus is another symptom that is characterized by alternating, rapid muscle contraction and relaxation. This presents itself as tremors and scissoring of the limbs. Distonia, or lasting muscle contractions and tightness, is also often experienced by those affected by spastic quadriplegia. These involuntary muscle contractions may affect the development of structural muscle around the hip and lead to hip dysplasia and dislocation, making it difficult to sit. The combination of these symptoms often makes it difficult for the patients to walk as well. Although the arms and legs of patients are often stiff, the neck is usually limp due to the lack of voluntary muscle control. Some adults have issues with sexual organs such as the ones that control the sphincter (anus) as well and bladder control. These can sometimes be treated with training and stimulation even if the problems have presented for years, some issues can be corrected in many cases with nutrition modification in 90 percent of cases, especially B12. Stimulation of the muscles involved can treat some forms of nerve damage, depending on what the issue is. Sexual issues can be difficult for those with this, and sexual acts and stimulation can correct most of the sexual issues.

Infants with spastic hemiplegia may develop a hand preference earlier than is typical.

Myoclonic seizures involve brief involuntary muscle twitching, and may become frequent enough to be disabling. Tonic-clonic seizures have two phases: the tonic phase may last a few seconds and involves the muscles tensing, and may lead to the person falling down; the clonic phase involves a convulsion of rapidly alternating muscle tensing and relaxing. Neurological dysfunction includes difficulty coordinating muscle movements (ataxia) and a decline in cognitive ability (dementia).

Benign neonatal seizures include two disorders benign idiopathic neonatal seizures and benign familial neonatal seizures. They are not classified as epilepsy. Anticonvulsants are not needed. And those affected do not develop epilepsy when they grow up.

Benign familial infantile epilepsy (BFIE), also known as benign familial infantile seizures (BFIS) or benign familial infantile convulsions (BFIC) is an epilepsy syndrome. Affected children, who have no other health or developmental problems, develop seizures during infancy. These seizures have focal origin within the brain but may then spread to become generalised seizures. The seizures may occur several times a day, often grouped in clusters over one to three days followed by a gap of one to three months. Treatment with anticonvulsant drugs is not necessary but they are often prescribed and are effective at controlling the seizures. This form of epilepsy resolves after one or two years, and appears to be completely benign. The EEG of these children, between seizures, is normal. The brain appears normal on MRI scan.

A family history of epilepsy in infancy distinguishes this syndrome from the non-familial classification (see benign infantile epilepsy), though the latter may be simply sporadic cases of the same genetic mutations. The condition is inherited with an autosomal dominant transmission. There are several genes responsible for this syndrome, on chromosomes 2, 16 and 19. It is generally described as idiopathic, meaning that no other neurological condition is associated with it or causes it. However, there are some forms that are linked to neurological conditions. One variant known as infantile convulsions and choreoathetosis (ICCA) forms an association between BFIE and paroxysmal kinesigenic choreoathetosis and has been linked to the PRRT2 gene on chromosome 16. An association with some forms of familial hemiplegic migraine (FHM) has also been found. Benign familial infantile epilepsy is not genetically related to benign familial neonatal epilepsy (BFNE), which occurs in neonates. However, a variation with seizure onset between two days and seven months called "benign familial neonatal–infantile seizures" (BFNIS) has been described, which is due to a mutation in the SCN2A gene.

In the early stages, it can be difficult to distinguish progressive myoclonic epilepsy from benign idiopathic generalised epilepsies, such as juvenile myoclonic epilepsy. With PME, the initial effectiveness of anticonvulsant treatment diminishes as seizures become more frequent and neurological decline progresses. However, these can also be signs of anticonvulsant intoxication. The myoclonus in PME is usually severe and is the prominent seizure type.

Familial hemiplegic migraine (FHM) is an autosomal dominant type of hemiplegic migraine that typically includes weakness of half the body which can last for hours, days or weeks. It can be accompanied by other symptoms, such as ataxia, coma and paralysis. There is clinical overlap in some FHM patients with episodic ataxia type 2 and spinocerebellar ataxia type 6, benign familial infantile epilepsy, and alternating hemiplegia of childhood. There are 3 known loci for FHM. FHM1, which accounts for approximately 50% of FHM patients, is caused by mutations in a gene coding for the P/Q-type calcium channel α subunit, CACNA1A. FHM1 is also associated with cerebellar degeneration. FHM2, which accounts for <25% of FHM cases, is caused by mutations in the /-ATPase gene ATP1A2. FHM3 is a rare subtype of FHM and is caused by mutations in a sodium channel α-subunit coding gene, SCN1A. These three subtypes do not account for all cases of FHM, suggesting the existence of at least one other locus (FHM4). Many of the non-familial cases of hemiplegic migraine (sporadic hemiplegic migraine) are also caused by mutations at these loci. A fourth gene that has been associated with this condition is the proline rich transmembrane protein 2 (PRRT2) - an axonal protein associated with the exocytosis complex. A fifth gene associated with this condition is SLC4A4 which encodes the electrogenic NaHCO3cotransporter NBCe1.

There are also non-familial cases of hemiplegic migraine, termed sporadic hemiplegic migraine. These cases seem to have the same causes as the familial cases and represent de novo mutations. Sporadic cases are also clinically identical to familial cases with the exception of a lack of family history of attacks.

Infantile convulsions and choreoathetosis (ICCA) syndrome is a neurological genetic disorder with an autosomal dominant mode of inheritance. It is characterized by the association of benign familial infantile epilepsy (BIFE) at age 3–12 months and later in life with paroxysmal kinesigenic choreoathetosis. The ICCA syndrome was first reported in 1997 in four French families from north-western France and provided the first genetic evidence for common mechanisms shared by benign infantile seizures and paroxysmal dyskinesia. The epileptic origin of PKC has long been a matter of debates and PD have been classified as reflex epilepsies.Indeed, attacks of PKC and epileptic seizures have several characteristics in common, they both are paroxysmal in presentation with a tendency to spontaneous remission, and a subset of PKC responds well to anticonvulsants. This genetic disease has been mapped to chromosome 16p-q12. More than 30 families with the clinical characteristics of ICCA syndrome have been described worldwide so far.

Seizures are purely occipital and primarily manifest with elementary visual hallucinations, blindness or both.

They are usually frequent and diurnal, develop rapidly within seconds and are brief, lasting from a few seconds to 1–3 min, and, rarely, longer.

Elementary visual hallucinations are the most common and characteristic ictal symptoms, and are most likely to be the first and often the only clinical manifestation. They consist mainly of small multicoloured circular patterns that often appear in the periphery of a visual field, becoming larger and multiplying during the course of the seizure, frequently moving horizontally towards the other side.

Other occipital symptoms, such as sensory illusions of ocular movements and ocular pain, tonic deviation of the eyes, eyelid fluttering or repetitive eye closures, may occur at the onset of the seizures or appear after the elementary visual hallucinations. "Deviation of the eyes", often associated with ipsilateral turning of the head, is the most common (in about 70% of cases) nonvisual ictal symptom. It is often associated with ipsilateral turning of the head and usually starts after visual hallucinations, although it may also occur while the hallucinations still persist. It may be mild, but more often it is severe and progresses to hemiconvulsions and secondarily generalised tonic clonic seizures (GTCS). Some children may have seizures of eye deviation from the start without visual hallucinations.

"Forced eyelid closure and eyelid blinking" occur in about 10% of patients, usually at a stage at which consciousness is impaired. They signal an impending secondarily GTCS.

"Ictal blindness", appearing from the start or, less commonly, after other manifestations of occipital seizures, usually lasts for 3–5 min. It can occur alone and be the only ictal event in patients who could, at other times, have visual hallucinations without blindness.

Complex visual hallucinations, visual illusions and other symptoms resulting from more anterior ictal spreading rarely occur from the start. They may terminate in hemiconvulsions or generalised convulsions.

Ictal headache, or mainly orbital pain, may occur and often precedes visual or other ictal occipital symptoms in a small number of patients.

Consciousness is not impaired during the visual symptoms (simple focal seizures), but may be disturbed or lost in the course of the seizure, usually before eye deviation or convulsions.

Occipital seizures of ICOE-G may rarely progress to extra-occipital manifestations, such as hemiparaesthesia. Spread to produce symptoms of temporal lobe involvement is exceptional and may indicate a symptomatic cause.

Post-ictal headache, mainly diffuse, but also severe, unilateral and pulsating, or indistinguishable from migraine headache, occurs in half the patients, in 10% of whom it may be associated with nausea and vomiting.

Circadian distribution: Visual seizures are predominantly diurnal and can occur at any time of the day. Longer seizures, with or without hemi or generalised convulsions, tend to occur either during sleep, causing the patient to wake up, or after awakening. Thus, some children may have numerous diurnal visual seizures and only a few seizures that are exclusively nocturnal or occur on awakening.

Frequency of seizures: If untreated, patients experience frequent and brief visual seizures (often several every day or weekly). However, propagation to other seizure manifestations, such as focal or generalised convulsions, is much less frequent.

Idiopathic childhood occipital epilepsy of Gastaut (ICOE-G) is a pure but rare form of idiopathic occipital epilepsy that affects otherwise normal children and adolescents. It is classified amongst benign idiopathic childhood focal epilepsies such as rolandic epilepsy and Panayiotopoulos syndrome.

This lesion is usually unilateral and affects several structures in the midbrain including:

It is caused by midbrain infarction as a result of occlusion of the paramedian branches of the posterior cerebral artery or of basilar bifurcation perforating arteries.

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).