Hemispatial neglect, also called hemiagnosia, hemineglect, unilateral neglect, spatial neglect, contralateral neglect, unilateral visual inattention, hemi-inattention, neglect syndrome or contralateral hemispatialagnosia, is a neuropsychological condition in which, after damage to one hemisphere of the brain is sustained, a deficit in attention to and awareness of one side of the field of vision is observed. It is defined by the inability of a person to process and perceive stimuli on one side of the body or environment, where that inability is not due to a lack of sensation. Hemispatial neglect is very commonly contralateral to the damaged hemisphere, but instances of ipsilesional neglect (on the same side as the lesion) have been reported.

Neglect is a heterogenous disorder that manifests itself radically differently in different patients. No single mechanism can account for these different manifestations. A vast array of impaired mechanisms are found in neglect. These mechanisms alone would not cause neglect. The complexity of attention alone—just one of several mechanisms that may interact—has generated multiple competing hypothetical explanations of neglect. So it is not surprising that it has proven difficult to assign particular presentations of neglect to specific neuroanatomical loci. Despite such limitations, we may loosely describe unilateral neglect with four overlapping variables: type, range, axis, and orientation.

Disconnection syndrome is a general term for a number of neurological symptoms caused by damage to the white matter axons of communication pathways—via lesions to association fibers or commissural fibers—in the cerebrum, independent of any lesions to the cortex. The behavioral effects of such disconnections are relatively predictable in adults. Disconnection syndromes usually reflect circumstances where regions A and B still have their functional specializations except in domains that depend on the interconnections between the two regions.

Callosal syndrome, or split-brain, is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms. Other types of disconnection syndrome include conduction aphasia (lesion of the association tract connecting Broca’s area and Wernicke’s), agnosia, apraxia, pure alexia, etc.

Allochiria (from the Greek meaning "other hand") is a neurological disorder in which the patient responds to stimuli presented to one side of their body as if the stimuli had been presented at the opposite side. It is associated with spatial s, usually symmetrical, of stimuli from one side of the body (or of the space) to the opposite one. Thus a touch to the left side of the body will be reported as a touch to the right side, which is also known as somatosensory allochiria. If the auditory or visual senses are affected, sounds (a person's voice for instance) will be reported as being heard on the opposite side to that on which they occur and objects presented visually will be reported as having been presented on the opposite side. Often patients may express allochiria in their drawing while copying an image. Allochiria often co-occurs with unilateral neglect and, like hemispatial neglect, the disorder arises commonly from damage to the right parietal lobe.

Allochiria is often confused with alloesthesia, also known as false allochiria. True allochiria is a symptom of dyschiria and unilateral neglect. Dyschiria is a disorder in the localization of sensation due to various degrees of dissociation and cause impairment in one side causing the inability to tell which side of the body was touched.

Alien hand syndrome (AHS) is a condition in which a person experiences their limbs acting seemingly on their own, without control over the actions. The term is used for a variety of clinical conditions and most commonly affects the left hand. There are many similar names used to describe the various forms of the condition but they are often used inappropriately. The afflicted person may sometimes reach for objects and manipulate them without wanting to do so, even to the point of having to use the controllable hand to restrain the alien hand. While under normal circumstances, thought, as intent, and action can be assumed to be deeply mutually entangled, the occurrence of alien hand syndrome can be usefully conceptualized as a phenomenon reflecting a functional "disentanglement" between thought and action.

Alien hand syndrome is best documented in cases where a person has had the two hemispheres of their brain surgically separated, a procedure sometimes used to relieve the symptoms of extreme cases of epilepsy and epileptic psychosis, e.g., temporal lobe epilepsy. It also occurs in some cases after brain surgery, stroke, infection, tumor, aneurysm, migraine and specific degenerative brain conditions such as Alzheimer's disease and Creutzfeldt–Jakob disease. Other areas of the brain that are associated with alien hand syndrome are the frontal, occipital, and parietal lobes.

Mobility can be difficult for people with homonymous hemianopsia. “Patients frequently complain of bumping into obstacles on the side of the field loss, thereby bruising their arms and legs.”

People with homonymous hemianopsia often experience discomfort in crowds. “A patient with this condition may be unaware of what he or she cannot see and frequently bumps into walls, trips over objects or walks into people on the side where the visual field is missing.”

A related phenomenon is Hemispatial neglect, the possible neglect of the right or left. The patient is not conscious of its existence. The right side of the face is not shaven, make up is applied to one side of the face only and only half of a plate of food is eaten. This, however, is not necessarily due to a sensory abnormality, and is therefore distinct from hemianopsia.

Hemianopsia or hemianopia is a visual field loss on the left or right side of the vertical midline. It can affect one eye but usually affects both eyes. Homonymous hemianopsia, or homonymous hemianopia, is hemianopic visual field loss on the same side of both eyes. Homonymous hemianopsia occurs because the right half of the brain has visual pathways for the left hemifield of both eyes, and the left half of the brain has visual pathways for the right hemifield of both eyes. When one of these pathways is damaged, the corresponding visual field is lost.

Allochiria has been observed mainly in the context of neglect which is usually due to a lesion that affects the right parietal lobe. In patients with allochiria, their sensibility is retained completely but the patient is not clear as to which side of the body has been touched. Their power of localization is retained but error exists to the side touched and they often refer the irritation to the corresponding part of the limb. In the patients' mind there is doubt or error as to which side of the body is touched.

There are multiple definitions of allochiria. According to Musser, allochiria is the reference of a sensory stimulus to the corresponding location on the opposite location on the opposite side of the body. Judson Bury says that a patient may refer to an impression on one side to a corresponding place on the opposite side of the body. Thus, if a patient is pricked on one limb, he may say that he feels it on the other. Overall, even though different author's definition differs on points such as the type of stimulus, and the symmetry between the site of the stimulus and the seat of its localization, they all agree that an essential feature of allochiria is the deflection of a sensation to the wrong side of the body, which is true allochiria. In none of these definitions is any stress laid on the state of the patient's knowledge of a right or left side and the symptoms are seen as an error in localization.

Obsersteiner laid stress that there is in allochiria no defect in vertical localization but merely confusion in the patient's mind between the opposite sides of the body and come to look upon the symptom as simply any form of bad mistake in localization.

There is in the patient's mind doubt or error as to the side touched while sensibility including the power of localization is otherwise retained. Allochiria has been described as occurring in nerve lesions, Hemiplegia, disseminated sclerosis Multiple sclerosis, tabes dorsalis, unilateral injury to the spinal cord, Ménière's disease, hysteria, symmetrical gangrene, and in connection with touch, pain, the "muscle sense," the temperature sense, sight, smell, taste, hearing, and the electrical reactions.

Allochiria can occur in relation to any or every segment of the body. In some cases allochiria may be , and in others it may be restricted to certain regions of the body, or even only to one part of the body. Allochiria is marked to have connections with a variety of senses and sometimes only certain kinds of stimuli can arouse the appropriate feeling of one sidedness.

The common emerging factor in alien hand syndrome is that the primary motor cortex controlling hand movement is isolated from premotor cortex influences but remains generally intact in its ability to execute movements of the hand.

A 2009 fMRI study looking at the temporal sequence of activation of components of a cortical network associated with voluntary movement in normal individuals demonstrated "an anterior-to-posterior temporal gradient of activity from supplemental motor area through premotor and motor cortices to the posterior parietal cortex". Therefore, with normal voluntary movement, the emergent sense of agency appears to be associated with an orderly sequence of activation that develops initially in the anteromedial frontal cortex in the vicinity of the supplementary motor complex on the medial surface of the frontal aspect of the hemisphere (including the supplementary motor area) "prior" to activation of the primary motor cortex in the pre-central gyrus on the lateral aspect of the hemisphere, when hand movement is being generated. Activation of the primary motor cortex, presumed to be directly involved in the execution of the action via projections into the corticospinal component of the pyramidal tracts, is then followed by activation of the posterior parietal cortex, possibly related to the receipt of recurrent or "re-afferent" somatosensory feedback generated from the periphery by the movement which would normally interact with the efference copy transmitted from primary motor cortex to permit the movement to be recognized as self-generated rather than imposed by an external force. That is, the efference copy allows the recurrent afferent somatosensory flow from the periphery associated with the self-generated movement to be recognized as "re-afference" as distinct from "ex-afference". Failure of this mechanism may lead to a failure to distinguish between self-generated and externally generated movement of the limb. This anomalous situation in which re-afference from a self-generated movement is mistakenly registered as ex-afference due to a failure to generate and successfully transmit an efference copy to sensory cortex, could readily lead to the interpretation that what is in actuality a self-generated movement has been produced by an external force as a result of the failure to develop a sense of agency in association with emergence of the self-generated movement (see below for a more detailed discussion).

A 2007 fMRI study examining the difference in functional brain activation patterns associated with alien as compared to non-alien "volitional" movement in a patient with alien hand syndrome found that alien movement involved anomalous "isolated" activation of the primary motor cortex in the damaged hemisphere contralateral to the alien hand, while non-alien movement involved the normal process of activation described in the preceding paragraph in which primary motor cortex in the intact hemisphere activates in concert with frontal premotor cortex and posterior parietal cortex presumably involved in a normal cortical network generating premotor influences on the primary motor cortex along with immediate post-motor re-afferent activation of the posterior parietal cortex.

Combining these two fMRI studies, one could hypothesize that the alien behavior that is unaccompanied by a sense of agency emerges due to autonomous activity in the primary motor cortex acting independently of premotor cortex pre-activating influences that would normally be associated with the emergence of a sense of agency linked to the execution of the action.

As noted above, these ideas can also be linked to the concept of efference copy and "re-afference", where efference copy is a signal postulated to be directed from premotor cortex (activated normally in the process associated with emergence of an internally generated movement) over to somatosensory cortex of the parietal region, in advance of the arrival of the "re-afferent" input generated from the moving limb, that is, the afferent return from the moving limb associated with the self-generated movement produced. It is generally thought that a movement is recognized as internally generated when the efference copy signal effectively "cancels out" the re-afference. The afferent return from the limb is effectively correlated with the efference copy signal so that the re-afference can be recognized as such and distinguished from "ex-afference", which would be afferent return from the limb produced by an externally imposed force. When the efference copy is no longer normally generated, then the afferent return from the limb associated with the self-generated movement is mis-perceived as externally produced "ex-afference" since it is no longer correlated with or canceled out by the efference copy. As a result, the development of the sense that a movement is not internally generated even though it actually is (i.e. the failure of the sense of agency to emerge in conjunction with the movement), could indicate a failure of the generation of the efference copy signal associated with the normal premotor process through which the movement is prepared for execution.

Since there is no disturbance of the "sense of ownership" of the limb (a concept discussed in the Wikipedia entry on sense of agency) in this situation, and there is no clearly apparent physically ostensible explanation for how the owned limb could be moving in a purposive manner without an associated sense of agency, effectively through its own power, a cognitive dissonance is created which may be resolved through the assumption that the goal-directed limb movement is being directed by an "alien" unidentifiable external force with the capacity for directing goal-directed actions of one's own limb.

Strokes are one of the most common causes of Foix-Chavany-Marie Syndrome. The type of strokes associated with this syndrome include embolic and thrombotic strokes. Strokes affecting the middle cerebral artery and the branches that pass through or near the operculum are characteristic of FCMS.

Symptoms of infections specifically HIV and Herpes simplex encephalitis can cause FCMS. Numerous lesions can develop with HIV infections, which likely result in the development of FCMS.

Cerebellar cognitive affective syndrome (CCAS), also called "Schmahmann's syndrome" is a condition that follows from lesions (damage) to the cerebellum of the brain. This syndrome, described by Dr. Jeremy Schmahmann and his colleagues refers to a constellation of deficits in the cognitive domains of executive function, spatial cognition, language, and affect resulting from damage to the cerebellum. Impairments of executive function include problems with planning, set-shifting, abstract reasoning, verbal fluency, and working memory, and there is often perseveration, distractibility and inattention. Language problems include dysprosodia, agrammatism and mild anomia. Deficits in spatial cognition produce visual–spatial disorganization and impaired visual–spatial memory. Personality changes manifest as blunting of affect or disinhibited and inappropriate behavior. These cognitive impairments result in an overall lowering of intellectual function. CCAS challenges the traditional view of the cerebellum being responsible solely for regulation of motor functions. It is now thought that the cerebellum is responsible for monitoring both motor and nonmotor functions. The nonmotor deficits described in CCAS are believed to be caused by dysfunction in cerebellar connections to the cerebral cortex and limbic system.

Quadrantanopia, quadrantanopsia, or quadrant anopia refers to an anopia affecting a quarter of the field of vision.

It can be associated with a lesion of an optic radiation. While quadrantanopia can be caused by lesions in the temporal and parietal lobes, it is most commonly associated with lesions in the occipital lobe.

Many studies have shown that disconnection syndromes such as aphasia, agnosia, apraxia, pure alexia and many others are not caused by direct damage to functional neocortical regions. They can also be present on only one side of the body which is why these are categorized as hemispheric disconnections. The cause for hemispheric disconnection is if the interhemispheric fibers, as mentioned earlier, are cut or reduced.

An example is commissural disconnect in adults which usually results from surgical intervention, tumor, or interruption of the blood supply to the corpus callosum or the immediately adjacent structures. Callosal disconnection syndrome is characterized by left ideomotor apraxia and left-hand agraphia and/or tactile anomia, and is relatively rare.

Other examples include commissurotomy, the surgical cutting of cerebral commissures to treat epilepsy and callosal agenesis which is when individuals are born without a corpus callosum. Those with callosal agenesis can still perform interhemispheric comparisons of visual and tactile information but with deficits in processing complex information when performing the respective tasks.

A somatosensory disorder is an impairment of the somatosensory system.

The CCAS has been described in both adults and children. The precise manifestations may vary on an individual basis, likely reflecting the precise location of the injury in the cerebellum. These investigators subsequently elaborated on the affective component of the CCAS, i.e., the neuropsychiatric phenomena. They reported that patients with injury isolated to the cerebellum may demonstrate distractibility, hyperactivity, impulsiveness, disinhibition, anxiety, ritualistic and stereotypical behaviors, illogical thought and lack of empathy, aggression, irritability, ruminative and obsessive behaviors, dysphoria and depression, tactile defensiveness and sensory overload, apathy, childlike behavior, and inability to comprehend social boundaries and assign ulterior motives.

The CCAS can be recognized by the pattern of deficits involving executive function, visual-spatial cognition, linguistic performance and changes in emotion and personality. Underdiagnosis may reflect lack of familiarity of this syndrome in the scientific and medical community. The nature and variety of the symptoms may also prove challenging. Levels of depression, anxiety, lack of emotion, and affect deregulation can vary between patients. The symptoms of CCAS are often moderately severe following acute injury in adults and children, but tend to lessen with time. This supports the view that the cerebellum is involved with the regulation of cognitive processes.

The absence of proprioception or two-point tactile discrimination on one side of the body suggests injury to the contralateral side of the primary somatosensory cortex. However, depending on the extent of the injury, damage can range in loss of proprioception of an individual limb or the entire body. A deficit known as cortical astereognosis of the receptive type describes an inability to make use of tactile sensory information for identifying objects placed in the hand. For example, if this type of injury effects the hand region in the primary somatosensory cortex for one cerebral hemisphere, a patient with closed eyes cannot perceive the position of the fingers on the contralateral hand and will not be able to identify objects such as keys or a cell phone if they are placed into that hand.

Homonymous denotes a condition which affects the same portion of the visual field of each eye.

Homonymous inferior quadrantanopia is a loss of vision in the same lower quadrant of visual field in both eyes whereas a homonymous superior quadrantanopia is a loss of vision in the same upper quadrant of visual field in both eyes.

A lesion affecting one side of the temporal lobe may cause damage to the inferior optic radiations (known as the temporal pathway or Meyer's loop) which can lead to superior quadrantanopia on the contralateral side of both eyes (colloquially referred to as "pie in the sky"); if the superior optic radiations (parietal pathway) are lesioned, the visual loss occurs on the inferior contralateral side of both eyes and is referred to as an inferior quadrantanopia.

The prognosis of a lesion in the visual neural pathways that causes a conjugate gaze palsy varies greatly. Depending on the nature of the lesion, recovery may happen rapidly or recovery may never progress. For example, optic neuritis, which is caused by inflammation, may heal in just weeks, while patients with an ischemic optic neuropathy may never recover.

Conjugate gaze palsies are neurological disorders affecting the ability to move both eyes in the same direction. These palsies can affect gaze in a horizontal, upward, or downward direction. These entities overlap with ophthalmoparesis and ophthalmoplegia.

Internuclear ophthalmoplegia (INO) is a disorder of conjugate lateral gaze in which the affected eye shows impairment of adduction. When an attempt is made to gaze contralaterally (relative to the affected eye), the affected eye adducts minimally, if at all. The contralateral eye abducts, however with nystagmus. Additionally, the divergence of the eyes leads to horizontal diplopia. That is, if the right eye is affected the patient will "see double" when looking to the left, seeing two images side-by-side. Convergence is generally preserved.

Posterior cerebral artery syndrome is a condition whereby the blood supply from the posterior cerebral artery (PCA) is restricted, leading to a reduction of the function of the portions of the brain supplied by that vessel: the occipital lobe, the inferomedial temporal lobe, a large portion of the thalamus, and the upper brainstem and midbrain.

This event restricts the flow of blood to the brain in a near-immediate fashion. The blood hammer is analogous to the water hammer in hydrology and it consists of a sudden increase of the upstream blood pressure in a blood vessel when the bloodstream is abruptly blocked by vessel obstruction. Complete understanding of the relationship between mechanical parameters in vascular occlusions is a critical issue, which can play an important role in the future diagnosis, understanding and treatment of vascular diseases.

Depending upon the location and severity of the occlusion, signs and symptoms may vary within the population affected with PCA syndrome. Blockages of the proximal portion of the vessel produce only minor deficits due to the collateral blood flow from the opposite hemisphere via the posterior communicating artery. In contrast, distal occlusions result in more serious complications. Visual deficits, such as agnosia, prosopagnosia or cortical blindness (with bilateral infarcts) may be a product of ischemic damage to occipital lobe. Occlusions of the branches of the PCA that supply the thalamus can result in central post-stroke pain and lesions to the subthalamic branches can produce “a wide variety of deficits”.

Left posterior cerebral artery syndrome presents alexia without agraphia; the lesion is in the splenium of the corpus callosum.

An occurrence of Todd's paralysis indicates that a seizure has occurred. The prognosis for the patient depends upon the effects of the seizure, not the occurrence of the paralysis.

The disorder is caused by injury or dysfunction in the medial longitudinal fasciculus (MLF), a heavily myelinated tract that allows conjugate eye movement by connecting the paramedian pontine reticular formation (PPRF)-abducens nucleus complex of the contralateral side to the oculomotor nucleus of the ipsilateral side.

In young patients with bilateral INO, multiple sclerosis is often the cause. In older patients with one-sided lesions a stroke is a distinct possibility. Other causes are possible.

The cause of Todd's paresis been attributed to the affected cortex being ‘exhausted’ or silenced due to increased inhibition, but these conjectures are not supported. It has been observed that the impairments that follow seizures are similar to those that follow strokes, where for a period of time blood flow to certain areas of the brain is restricted and these areas are starved of oxygen.