How does agnosia affect the brain?
Apperceptive agnosia
Each patient that suffers from apperceptive agnosia does not have brain damage in exactly the same area. However, brain damage in proximity to the occipital lobe is largely correlated with the patterns of deficit seen in apperceptive agnosics. For example, patient JB suffered extensive damage to the parietal-occipital areas to the left cerebral hemisphere leading to his deficit in the ability to name distinguish between structurally similar object.
Human brain
Although the human brain represents only 2% of the body weight, it receives 15% of the cardiac output, 20% of total body oxygen consumption, and 25% of total body glucose utilization. The brain mostly uses glucose for energy, and deprivation of glucose, as can happen in hypoglycemia, can result in loss of consciousness. The energy consumption of the brain does not vary greatly over time, but active regions of the cortex consume somewhat more energy than inactive regions: this fact forms the basis for the functional brain imaging methods PET and fMRI. These functional imaging techniques provide a three-dimensional image of metabolic activity.
Apperceptive agnosia
Visual apperceptive agnosia is a visual impairment that results in a patient's inability to name objects. While agnosics suffer from severe deficits, patients' visual acuity and other visual abilities such as perceiving parts and colours remain intact. Deficits seem to occur because of damage to early-level perceptual processing. While patients are able to effectively allocate attention to locate the object and perceive the parts, they are unable to group together the parts they see and name the object accurately. This is demonstrated by the fact that patients are more effective at naming two attributes from a single object than they are able to name one attribute on each of the two superimposed objects. In addition they are still able to describe objects in detail and recognize objects by touch.
Apperceptive agnosia
Tactile apperceptive agnosia results in the inability to shape representations specific to tactile modality. The impairment is restricted to the hands even though sensation is not impaired. This is similar to visual apperceptive agnosia in that it is a basic level of processing that is impaired. Some individuals are unable to recognize objects by touch because of a small cerebral infarction.
Scholarly approaches to mysticism
Andrew B. Newberg and Eugene G. d'Aquili, in their book "Why God Won't Go Away: Brain Science and the Biology of Belief", take a perennial stance, describing their insights into the relationship between religious experience and brain function. d'Aquili describes his own meditative experiences as "allowing a deeper, simpler part of him to emerge", which he believes to be "the truest part of who he is, the part that never changes." Not content with personal and subjective descriptions like these, Newberg and d'Aquili have studied the brain-correlates to such experiences. They scanned the brain blood flow patterns during such moments of mystical transcendence, using SPECT-scans, to detect which brain areas show heightened activity. Their scans showed unusual activity in the top rear section of the brain, the "posterior superior parietal lobe", or the "orientation association area (OAA)" in their own words. This area creates a consistent cognition of the physical limits of the self. This OAA shows a sharply reduced activity during meditative states, reflecting a block in the incoming flow of sensory information, resulting in a perceived lack of physical boundaries. According to Newberg and d'Aquili, 
Newberg and d'Aquili conclude that mystical experience correlates to observable neurological events, which are not outside the range of normal brain function. They also believe that 
"Why God Won't Go Away" "received very little attention from professional scholars of religion". According to Bulkeley, "Newberg and D'Aquili seem blissfully unaware of the past half century of critical scholarship questioning universalistic claims about human nature and experience". Matthew Day also notes that the discovery of a neurological substrate of a "religious experience" is an isolated finding which "doesn't even come close to a robust theory of religion".
Brain damage
Damage to the Broca’s area typically produces symptoms like omitting functional words (agrammatism), sound production changes, dyslexia, dysgraphia, and problems with comprehension and production. Broca’s aphasia is indicative of damage to the posterior inferior frontal gyrus of the brain.
Apperceptive agnosia
Apperceptive agnosia is a failure in recognition that is due to a failure of perception. In contrast, associative agnosia is a type of agnosia where perception occurs but recognition still does not occur. When referring to apperceptive agnosia, visual and object agnosia are most commonly discussed; This occurs because apperceptive agnosia is most likely to present visual impairments. However, in addition to visual apperceptive agnosia there are also cases of apperceptive agnosia in other sensory areas.
Auditory agnosia
The term auditory agnosia was originally coined by Freud (1891) to describe patients with selective impairment of environmental sounds. In a review of the auditory agnosia literature, Ulrich re-named this disorder as non-verbal auditory agnosia (although sound auditory agnosia and environmental sound auditory agnosia are also commonly used). This disorder is very rare and only 18 cases have been documented. In contradiction to pure word deafness and general auditory agnosia, this disorder is likely under-diagnosed because patients are often not aware of their disorder, and thus don’t seek medical intervention.
Amusia
Other than their inability to hear music, which is most likely due to a genetic defect, the rest of an amusic's brain remains normal. The only effect is on the ability to tell different notes apart due to the separation of two key areas in the brain. Most sufferers of amusia describe music as unpleasant. Others simply refer to it as noise and find it annoying. This can have social implications because amusics often try to avoid music, which in many social situations is not an option. In China and other countries in which identical words have different meanings based on pitch, amusia may have a much more pronounced social and emotional impact: difficulty in speaking and understanding the language.
Visual agnosia
The two main categories of visual agnosia are:Patient C.K. was born in 1961 in England and emigrated to Canada in 1980. In January of 1988, C.K. sustained a head injury from a motor vehicle accident while out for a jog. Following the accident, C.K. experienced many cognitive issues, mood swings, poor memory, and temper outbursts. C.K. also had motor weakness on the left side and a left homonymous hemianopia. He recovered well, retaining normal intelligence and normal visual acuity. He was able to complete a Masters in History, later working as a manager at a large corporation. Although his recovery was successful in other areas of cognition, C.K. still struggles to make sense of the visual world.
Self-awareness
Anosognosia was a term coined by Joseph Babinski to describe the clinical condition in which an individual suffered from left hemiplegia following a right cerebral hemisphere stroke yet denied that there were any problems with their left arm or leg. This condition is known as anosognosia for hemiplegia (AHP). This condition has evolved throughout the years and is now used to describe people who lack subjective experience in both neurological and neuropsychological cases. A wide variety of disorders are associated with anosognosia. For example, patients who are blind from cortical lesions might in fact be unaware that they are blind and may state that they do not suffer from any visual disturbances. Individuals with aphasia and other cognitive disorders may also suffer from anosognosia as they are unaware of their deficiencies and when they make certain speech errors, they may not correct themselves due to their unawareness. Individuals who suffer from Alzheimer's disease lack awareness; this deficiency becomes more intense throughout their disease. A key issue with this disorder is that people who do have anosognosia and suffer from certain illnesses may not be aware of them, which ultimately leads them to put themselves in dangerous positions and/or environments. To this day there are still no available treatments for AHP, but it has been documented that temporary remission has been used following vestibular stimulation.
Amygdala
With advances in neuroimaging technology such as MRI, neuroscientists have made significant findings concerning the amygdala in the human brain. A variety of data shows the amygdala has a substantial role in mental states, and is related to many psychological disorders. Some studies have shown children with anxiety disorders tend to have a smaller left amygdala. In the majority of the cases, there was an association between an increase in the size of the left amygdala with the use of SSRIs (antidepressant medication) or psychotherapy. The left amygdala has been linked to social anxiety, obsessive and compulsive disorders, and post traumatic stress, as well as more broadly to separation and general anxiety. In a 2003 study, subjects with borderline personality disorder showed significantly greater left amygdala activity than normal control subjects. Some borderline patients even had difficulties classifying neutral faces or saw them as threatening. Individuals with psychopathy show reduced autonomic responses to instructed fear cues than otherwise healthy individuals. In 2006, researchers observed hyperactivity in the amygdala when patients were shown threatening faces or confronted with frightening situations. Patients with severe social phobia showed a correlation with increased response in the amygdala. Similarly, depressed patients showed exaggerated left amygdala activity when interpreting emotions for all faces, and especially for fearful faces. This hyperactivity was normalized when patients were administered antidepressant medication. By contrast, the amygdala has been observed to respond differently in people with bipolar disorder. A 2003 study found that adult and adolescent bipolar patients tended to have considerably smaller amygdala volumes and somewhat smaller hippocampal volumes. Many studies have focused on the connections between the amygdala and autism.
Mechanism of anoxic depolarization in the brain
During brain ischemia, glutamate is released in excess from the presynaptic terminal, leading to the uncontrollable opening of the glutamate receptors, including the NMDA and AMPA receptors, which allows for an excessive influx of Ca into the intracellular environment. Purinergic and NMDA receptors activate the pannexin-1 channels, which become hyperactive and allow the release of ATP from the intracellular environment. As the extracellular glutamate and ATP increase, several complexes are activated and converge into apoptotic and necrotic cascade pathways, which cause neuronal damage and death.
Disconnection syndrome
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.
Tip of the tongue
Anomic aphasia is the inability to recall words and names and is a common symptom of patients with Aphasia and Alzheimer's disease (AD). Research has been conducted to find out how these particular diseases affect TOTs in these individuals. In a study by Beeson, Holland, and Murray (1997), participants with Alzheimer's disease and three classic aphasic syndromes (Broca’s, anomic, and conduction aphasia) were instructed to name famous people. Those with anomic aphasia showed to be superior to the other groups in their ability to naming famous people that were presented. This finding was expected as the group has relatively mild aphasia. However, the Broca’s conduction and AD groups did not differ in immediate or delayed naming of famous faces. All of the groups provided some basic identifying semantic information for at least half of the items presented, suggesting a fair number of items potentially in TOT. Conduction and Broca’s groups showed strongest evidence of TOT, performing better than the other groups in identification of initial letters.
Hellblade: Senua's Sacrifice
Antoniades admitted that during his research, he "didn't have to look very far to discover my own ignorance of the subject". To portray psychosis properly, Ninja Theory "consulted world-leading neuroscientists and non-profit organizations like Wellcome Trust to properly capture the experience of psychosis and its devastating effects on the human mind". Antoniades "learnt that people can experience hallucinations and delusional beliefs without it being a problem – the illness comes when those experiences cause suffering. Often the recovery is not about curing yourself of hallucinations, but finding ways to live with them. That was a revelation to me".
Effects of cannabis
When THC enters the blood stream and reaches the brain, it binds to cannabinoid receptors. The endogenous ligand of these receptors is anandamide, the effects of which THC emulates. This agonism of the cannabinoid receptors results in changes in the levels of various neurotransmitters, especially dopamine and norepinephrine; neurotransmitters which are closely associated with the acute effects of cannabis ingestion, such as euphoria and anxiety.
Some effects may include a general alteration of conscious perception, euphoria, feelings of well-being, relaxation or stress reduction, increased appreciation of the arts, including humor and music (especially discerning its various components/instruments), joviality, metacognition and introspection, enhanced recollection (episodic memory), increased sensuality, increased awareness of sensation, increased libido, and creativity. Abstract or philosophical thinking, disruption of linear memory and paranoia or anxiety are also typical. Anxiety is the most commonly reported side effect of smoking marijuana. Between 20 and 30 percent of recreational users experience intense anxiety and/or panic attacks after smoking cannabis, however, some report anxiety only after not smoking cannabis for a prolonged period of time. Inexperience and use in an unfamiliar environment are major contributing factors to this anxiety. Cannabidiol (CBD), another cannabinoid found in cannabis in varying amounts, has been shown to ameliorate the adverse effects of THC, including anxiety, that some consumers experience.
Asemia
The most common cause of asemia is brain damage, such as a stroke or a brain tumor. Other possible causes include Alzheimer's disease and infection. Roger Wolcott Sperry, through his research of split-brain patients, had found out that the human brain lateralizes functions, meaning that the two hemispheres of the brain have different functions. Brain damage, specifically to the left hemisphere, can impair our ability to speak or understand language. This led Sperry to conclude that due to the lateralization of brain function, language is based in the left hemisphere. Therefore, any kind of brain damage to the left hemisphere will greatly impact language, whether it is expressive or receptive.
Agnosia
In order to assess an individual for agnosia, it must be verified that the individual is not suffering from a loss of sensation, and that both their language abilities and intelligence are intact. In order for an individual to be diagnosed with agnosia, they must only be experiencing a sensory deficit in a single modality. To make a diagnosis, the distinction between apperceptive and associative agnosia must be made. This distinction can be made by having the individual complete copying and matching tasks. If the individual is suffering from a form of apperceptive agnosia they will not be able to match two stimuli that are identical in appearance. In contrast, if an individual is suffering from a form of associative agnosia, they will not be able to match different examples of a stimulus. For example, an individual who has been diagnosed with associative agnosia in the visual modality would not be able to match pictures of a laptop that is open with a laptop that is closed.
Associative visual agnosia
Teuber described the associative agnostic as having a "percept stripped of its meaning," because the afflicted individual cannot generate unique semantic information to identify the percept, since though it is fully formed, it fails to activate the semantic memory associated with the stimulus. Warrington (1975) offered that the problem lies in impaired access to generic engrams (memory traces) that describe categories of objects made up of a multitude of similar elements. Essentially, damage to a modality-specific meaning process (semantic system), is proposed, either in terms of defective access to or a degradation of semantic memory store for visual semantic representations themselves. The fact that agnosias are often restricted to impairments of particular types of stimuli, within distinct sensory modalities, suggests that there are separate modality specific pathways for the meaningful representation of objects and pictures, written material, familiar faces, and colors.
Altered state of consciousness
Alcohol alters consciousness by shifting levels of neurotransmitters. Neurotransmitters are endogenous chemicals that transmit signals across a synapse from one neuron (nerve cell) to another "target" cell (often another neuron). Neurotransmitters can cause inhibitory or excitatory effects on the "target" cell they are affecting. Alcohol increases the effect of the neurotransmitter GABA (gamma-Aminobutyric acid) in the brain. GABA causes slow actions and inaudible verbal communication that often occur in alcoholics (Berridge, V 2001). Alcohol also decreases the excitatory neurotransmitter glutamate. Suppressing this stimulant results in a similar type of physiological slowdown. In addition to increasing the GABA and decreasing the glutamate in the brain, alcohol increases the amount of the chemical dopamine in the brain, which is one of the addictive causes of alcoholism.
Social-emotional agnosia
Damage to the right temporal occipital region in humans has been associated with the inability to recognize the faces of loved ones, friends, and pets (considered a form of prosopagnosia). This limits the ability to appropriately interact with familiar people, potentially severely damaging interpersonal relationships. People with social-emotional agnosia may distance themselves from interacting with other people and prefer isolation. Maternal behavior is also severely affected, causing mothers to fail to recognize their children as their own. In human children, deficits in imitating and responding to peer social interactions have been observed. Children with this agnosia have also been found to have hyperorality, an increased tendency to investigate objects with their mouths, which is also a common symptom of Klüver-Bucy syndrome.
Amusia
Amusia can also be related to aprosody, a disorder in which the sufferer's speech is affected, becoming extremely monotonous. It has been found that both amusia and aprosody can arise from seizures occurring in the non-dominant hemisphere. They can also both arise from lesions to the brain, as can Broca's aphasia come about simultaneously with amusia from injury. There is a relation between musical abilities and the components of speech, however, they are not understood very well.
Associative visual agnosia
An agnosia that affects hearing, "auditory sound agnosia", is broken into subdivisions based on level of processing impaired, and a "semantic-associative" form is investigated within the auditory agnosias.
Societal and cultural aspects of autism
Two traits sometimes found in AS individuals are mind-blindness (the inability to predict the beliefs and intentions of others) and alexithymia (the inability to identify and interpret emotional signals in oneself or others), which reduce the ability to be empathetically attuned to others. Alexithymia in AS functions as an independent variable relying on different neural networks than those implicated in theory of mind. In fact, lack of Theory of Mind in AS may be a result of a lack of information available to the mind due to the operation of the alexithymic deficit.
Anosodiaphoria
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.
Alcoholism
Long-term misuse of alcohol can cause a wide range of mental health problems. Severe cognitive problems are common; approximately 10 percent of all dementia cases are related to alcohol consumption, making it the second leading cause of dementia. Excessive alcohol use causes damage to brain function, and psychological health can be increasingly affected over time. Social skills are significantly impaired in people suffering from alcoholism due to the neurotoxic effects of alcohol on the brain, especially the prefrontal cortex area of the brain. The social skills that are impaired by alcohol abuse include impairments in perceiving facial emotions, prosody perception problems and theory of mind deficits; the ability to understand humour is also impaired in alcohol abusers. Psychiatric disorders are common in alcoholics, with as many as 25 percent suffering severe psychiatric disturbances. The most prevalent psychiatric symptoms are anxiety and depression disorders. Psychiatric symptoms usually initially worsen during alcohol withdrawal, but typically improve or disappear with continued abstinence. Psychosis, confusion, and organic brain syndrome may be caused by alcohol misuse, which can lead to a misdiagnosis such as schizophrenia. Panic disorder can develop or worsen as a direct result of long-term alcohol misuse.
Alogia
Alogia is often considered a form of aphasia, which is a general impairment in linguistic ability. It often occurs with intellectual disability and dementia as a result of damage to the left hemisphere of the brain. People can revert to alogia as a way of reverse psychology, or avoiding questions.
Athetosis
Asphyxia directly causes basal ganglia damage due to lack of oxygen and therefore, insufficient nutrient supply. The lesions caused by asphyxia are most prominent on the caudate nucleus and the putamen. However, a less-studied consequence of the resulting hypoxia is its effect on the concentrations of the neurotransmitter dopamine within the synapses of neurons in the basal ganglia. Hypoxia leads to an increase in the extracellular dopamine levels and therefore, an increase in the activity of the dopaminergic neurons. Furthermore, this increase in extracellular concentration is not caused by an increase in the neurotransmitter synthesis, but instead on inhibiting its reuptake back into the neurons and glial cells. Therefore, there is an increased dopaminergic effect as dopamine remains in the synapse at higher concentrations leading to additional post-synaptic response. As a result, the uncontrollable writhing motions witnessed with athetosis deal with the over-activity of synapses within the basal ganglia.
Agnosia
Initially many individuals with a form of agnosia are unaware of the extent to which they have either a perceptual or recognition deficit. This may be caused by anosognosia which is the lack of awareness of a deficit. This lack of awareness usually leads to a form of denial and resistance to any form of help or treatment. There are various methods that can be used which can help the individual recognize the impairment in perception or recognition that they may have. A patient can be presented with a stimulus to the impaired modality only to help increase their awareness of their deficit. Alternatively, a task can be broken down into its component parts so that the individual can see each part of the problem caused by the deficit. Once the individual acknowledges their perceptual or recognition deficit, a form of treatment may be recommended. There are various forms of treatment such as compensatory strategies with alternate modalities, verbal strategies, alternate cues and organizational strategies.
Eating disorders and memory
Glucose is the preferred energy source for the brain, accounting for 25% of the body’s glucose consumption, despite being only 2% of the body’s total weight. Glucose, along with serotonin, have been found to have significant effects within the cingulate cortex, frontal lobe, temporal lobe, and parietal lobe regions of the brain, including in those with anorexia. Individuals with eating disorders such as bulimia and anorexia show lower neural metabolism of glucose, possibly due to neural consequences of the disorder and/or due to heightened anxiety or depression. Studies have indicated the importance of glucose on memory, showing that reduced levels of glucose in the brain impair an individual’s ability to retrieve memories. Most evidence suggests that severe negative impairments are due to long term, prolonged glucose deprivation or restriction, such as those seen in individuals affected by eating disorders, however effects have been studied on a more short-term basis with negative memory impairments seen in individuals who consumed breakfast compared to those who did not.
Selfish brain theory
In the first DFG funding period from 2004 to 2007 researchers from the Clinical Research Group “Selfish Brain: brain glucose and metabolic syndrome" expanded the scope of validity of the “Selfish Brain" theory in central aspects by carrying out experiments on healthy and diseased test subjects. The researchers in Luebeck found the following key results regarding the axioms of the theory:The special position of the brain during inanition (due to fasting or tumor disease) was already confirmed experimentally over 80 years ago: The body mass reduces, but the mass of the brain hardly reduces, if at all (see 3). Recently this axiom of the selfish brain theory was supported by work at the University of Luebeck involving state-of-the-art magnetic resonance procedures, e.g. during metabolic stress. The ATP content in the brain and musculature of test subjects was examined by a magnetic resonance technique while either an energy deficit or surplus was induced in the blood by insulin or glucose injection. In both situations a sufficiently high ATP-concentration was measured in the brain. The measured high-energy-rich substances changed throughout to the benefit of the brain and to the disadvantage of the body cells. The glucose-supply of the brain had priority despite the physical stress that was being endured (see 11).
Associative visual agnosia
The affected individual may not realize that they have a visual problem and may complain of becoming "clumsy" or "muddled" when performing familiar tasks such as setting the table or simple DIY.
Anosognosia, a lack of awareness of the deficit, is common and can cause therapeutic resistance. In some agnosias, such as prosopagnosia, awareness of the deficit is often present; however shame and embarrassment regarding the symptoms can be a barrier in admission of a deficiency. Because agnosias result from brain lesions, no direct treatment for them currently exists, and intervention is aimed at utilization of coping strategies by patients and those around them. Sensory compensation can also develop after one modality is impaired in agnostics
Mirrored-self misidentification
Viewing one's own facial reflection in the mirror causes neurological changes in the right inferior frontal gyrus, the right inferior occipital gyrus, the right inferior parietal lobe, and the right parietal area. These changes, which all occur in the right hemisphere, highlight the role of the right hemisphere in self-related cognition and processing and support the theory that the right hemisphere is the most likely substrate for the "self" in the brain. When the right hemisphere is damaged in any way, the patient will most likely lose the ability to recognize one's face - the most common feature of self-recognition. When paired with mirror agnosia or impaired facial processing, damage in any of these areas of the right hemisphere of the brain can lead to difficulties in self-recognition. Delusions such as mirrored-self misidentification can then develop.
Associative visual agnosia
Most cases have injury to the occipital and temporal lobes and the critical site of injury appears to be in the left occipito-temporal region, often with involvement of the splenium of the corpus callosum. The etiology of the cognitive impairment, as well the areas of the brain affected by lesions and stage of recovery are the primary determinants of the pattern of deficit. More generalized recognition impairments, such as, animate object deficits, are associated with diffuse hypoxic damage, like carbon monoxide poisoning; more selective deficits are correlated with more isolated damage due to focal stroke.
Fusiform face area
One case study of agnosia provided evidence that faces are processed in a special way. A patient known as C. K., who suffered brain damage as a result of a car accident, later developed object agnosia. He experienced great difficulty with basic-level object recognition, also extending to body parts, but performed very well at recognizing faces. A later study showed that C. K. was unable to recognize faces that were inverted or otherwise distorted, even in cases where they could easily be identified by normal subjects. This is taken as evidence that the fusiform face area is specialized for processing faces in a normal orientation.
Cerebral atrophy
Many diseases that cause cerebral atrophy are associated with dementia, seizures, and a group of language disorders called the aphasias. Dementia is characterized by a progressive impairment of memory and intellectual function that is severe enough to interfere with social and work skills. Memory, orientation, abstraction, ability to learn, visual-spatial perception, and higher executive functions such as planning, organizing and sequencing may also be impaired. Seizures can take different forms, appearing as disorientation, strange repetitive movements, loss of consciousness, or convulsions. Aphasias are a group of disorders characterized by disturbances in speaking and understanding language. Receptive aphasia causes impaired comprehension. Expressive aphasia is reflected in odd choices of words, the use of partial phrases, disjointed clauses, and incomplete sentences.
Consciousness
One of the most striking disorders of consciousness goes by the name anosognosia, a Greek-derived term meaning 'unawareness of disease'. This is a condition in which patients are disabled in some way, most commonly as a result of a stroke, but either misunderstand the nature of the problem or deny that there is anything wrong with them. The most frequently occurring form is seen in people who have experienced a stroke damaging the parietal lobe in the right hemisphere of the brain, giving rise to a syndrome known as hemispatial neglect, characterized by an inability to direct action or attention toward objects located to the left with respect to their bodies. Patients with hemispatial neglect are often paralyzed on the right side of the body, but sometimes deny being unable to move. When questioned about the obvious problem, the patient may avoid giving a direct answer, or may give an explanation that doesn't make sense. Patients with hemispatial neglect may also fail to recognize paralyzed parts of their bodies: one frequently mentioned case is of a man who repeatedly tried to throw his own paralyzed right leg out of the bed he was lying in, and when asked what he was doing, complained that somebody had put a dead leg into the bed with him. An even more striking type of anosognosia is Anton–Babinski syndrome, a rarely occurring condition in which patients become blind but claim to be able to see normally, and persist in this claim in spite of all evidence to the contrary.
Agnosía
A young woman, Joana Prats, suffers from agnosia, a strange, primary visual disease that is one of the neuropsychological disorders of perception. Although her eyes and ears are in perfect condition, her brain is not able to correctly interpret the stimuli it receives. Joana is the only person to know an industrial secret left behind by her late father and becomes the victim of a sinister plan to extract this information. Her captors plan to use her sensory condition to help extract the information that they so desperately want.Roxbury Pictures shot the film in December 2009 at Barcelona and Parc Nacional d'Aigüestortes Estany de Sant Maurici in Province of Lleida. It was the second film directed by producer Eugenio Miro and based on a screenplay by Antonio Trashorras. In the leads in the thriller acts Eduardo Noriega, Martina Gedeck, Bárbara Goenaga and Jack Taylor in his second feature film under Eugenio Mira.
Brain ischemia
The main symptoms involve impairments in vision, body movement, and speaking. The causes of brain ischemia vary from sickle cell anemia to congenital heart defects. Symptoms of brain ischemia can include unconsciousness, blindness, problems with coordination, and weakness in the body. Other effects that may result from brain ischemia are stroke, cardiorespiratory arrest, and irreversible brain damage.
Short-term effects of alcohol consumption
Alcohol has a powerful effect on glutamate as well. Alcohol decreases glutamate's ability to bind with NMDA and acts as an antagonist of the NMDA receptor, which plays a critical role in LTP by allowing Ca2+ to enter the cell. These inhibitory effects are thought to be responsible for the "memory blanks" that can occur at levels as low as 0.03% blood level. In addition, reduced glutamate release in the dorsal hippocampus has been linked to spatial memory loss. Chronic alcohol users experience an upregulation of NMDA receptors because the brain is attempting to reestablish homeostasis. When a chronic alcohol user stops drinking for more than 10 hours, apoptosis can occur due to excitotoxicity. The seizures experienced during alcohol abstinence are thought to be a result of this NMDA upregulation. Alteration of NMDA receptor numbers in chronic alcoholics is likely to be responsible for some of the symptoms seen in delirium tremens during severe alcohol withdrawal, such as delirium and hallucinations. Other targets such as sodium channels can also be affected by high doses of alcohol, and alteration in the numbers of these channels in chronic alcoholics is likely to be responsible for as well as other effects such as cardiac arrhythmia. Other targets that are affected by alcohol include cannabinoid, opioid and dopamine receptors, although it is unclear whether alcohol affects these directly or if they are affected by downstream consequences of the GABA/NMDA effects. People with a family history of alcoholism may exhibit genetic differences in the response of their NMDA glutamate receptors as well as the ratios of GABA subtypes in their brain. Alcohol inhibits sodium-potassium pumps in the cerebellum and this is likely how it corrupts cerebellar computation and body co-ordination.
Visual agnosia
Magnetic Resonance Imaging (MRI) showed bilateral thinning of C.K.’s Occipital Lobe which resulted in associative visual agnosia. Patients that suffer from visual agnosia are unable to identify visually presented objects. They can identify these objects through other modalities such as touch but if presented visually, they are unable to. Associative Agnosic patients cannot create a detailed representation of the visual world in their brains, they can only perceive elements of whole objects. They also cannot form associations between objects or assign meaning to objects.
Agnosia
Individuals with apperceptive visual agnosia display the ability to see contours and outlines when shown an object, but they experience difficulty if asked to categorize objects. Apperceptive visual agnosia is associated with damage to one hemisphere, specifically damage to the posterior sections of the right hemisphere.
Auditory agnosia
Auditory agnosia patients are often impaired in the discrimination of all sounds, including music. However, in two such patients music perception was spared and in one patient music perception was enhanced. The medical literature reports of 33 patients diagnosed with an exclusive deficit for the discrimination and recognition of musical segments (i.e., amusia). The damage in all these cases was localized to the right hemisphere or was bilateral. (with the exception of one case.) The damage in these cases tended to focus around the temporal pole. Consistently, removal of the anterior temporal lobe was also associated with loss of music perception, and recordings directly from the anterior auditory cortex revealed that in both hemispheres, music is perceived medially to speech. These findings therefore imply that the loss of music perception in auditory agnosia is because of damage to the medial anterior STG. In contrast to the association of amusia specific to recognition of melodies (amelodia) with the temporal pole, posterior STG damage was associated with loss of rhythm perception (arryhthmia). Conversely, in two patients rhythm perception was intact, while recognition/discrimination of musical segments was impaired. Amusia also dissociates in regard to enjoyment from music. In two reports, amusic patients, who weren’t able to distinguish musical instruments, reported that they still enjoy listening to music. On the other hand, a patient with left hemispheric damage in the amygdala was reported to perceive, but not enjoy, music.
Speech and language impairment
Acquired disorders result from brain injury, stroke or atrophy, many of these issues are included under the Aphasia umbrella.
Brain damage, for example, may result in various forms of aphasia if critical areas of the brain such as Broca's or Wernicke's area are damaged by lesions or atrophy as part of a dementia.
Cerebral hypoxia
Cerebral hypoxia can be caused by any event that severely interferes with the brain's ability to receive or process oxygen. This event may be internal or external to the body. Mild and moderate forms of cerebral hypoxia may be caused by various diseases that interfere with breathing and blood oxygenation. Severe asthma and various sorts of anemia can cause some degree of diffuse cerebral hypoxia. Other causes include status epilepticus, work in nitrogen-rich environments, ascent from a deep-water dive, flying at high altitudes in an unpressurized cabin without supplemental oxygen, and intense exercise at high altitudes prior to acclimatization.
Agnosia
The term 'agnosia' comes from the Ancient Greek ἀγνωσία ("agnosia"), "ignorance", "absence of knowledge". It was introduced by Sigmund Freud in 1891: "For disturbances in the recognition of objects, which Finkelnburg classes as asymbolia, I should like to propose the term 'agnosia'." Prior to Freud's introduction of the term, some of the first ideas about agnosia came from Carl Wernicke, who created theories about receptive aphasia in 1874. He noted that individuals with receptive aphasia did not possess the ability to understand speech or repeat words. He believed that receptive aphasia was due to lesions of the posterior third of the left superior temporal gyrus. Due to these lesions, Wernicke believed that individuals with receptive aphasia had a limited deafness for certain sounds and frequencies in speech.
Apperceptive agnosia
Apperceptive visual agnosia results in profound difficulties on a patient's ability to recognize visually presented information. Apperceptive agnosia affects the perceptual processing of individuals. Impairments of elements such as color and motion makes it difficult to interpret shape or the spatial arrangements of objects. Deficits in apperceptive agnosics have not been linked to deficits in acuity. Additionally, patients have an intact ability to attend to cued stimuli. They have the ability to maintain fixation, reach for moving targets, and write as well. Those with apperceptive agnosia, however, have difficultly copying geometric shapes and letters. In some cases individuals are able to trace letters and shapes with their finger but they are unable to use the technique as a strategy to name objects.
Social-emotional agnosia
Social-emotional agnosia is mainly caused by abnormal functioning in a particular brain area called the amygdala. Typically this agnosia is only found in people with bilateral amygdala damage; that is damage to amygdala regions in both hemispheres of the brain. It can be accompanied by right or bilateral temporal lobe damage. The amygdala dysfunction causes the inability to select appropriate behaviors in a specific social context. Symptoms can include reduced aggression, fearfulness, competitiveness, and social dominance. Those with social-emotional agnosia have difficulty discerning the emotional meaning and significance behind objects, which causes a loss of fondness and familiarity. Bilateral amygdala damage has also been associated with social unresponsiveness, leading to an avoidance of social interactions and a preference for isolation from their own species. Evidence suggests that damage to the amygdala and the limbic system (specifically the amygdala-hypothalamus pathway) results in the loss of the core ability to recognize and interpret the mental states of others, a vital ability in social interactions. The amygdala evokes highly personal emotional memories and the loss of this function causes hypo-emotionality, a general lack of emotion when presented with different stimuli. Hypersexuality has also been observed in those with disconnection in the amygdala-hypothalamus pathway. Temporal lobe epilepsy has been shown to cause bilateral amygdala damage which could result in symptoms similar to social-emotional agnosia, but the precise relationship between the two disorders is unknown.
Mixed transcortical aphasia
A stroke is one of the leading causes of disability in the United States. Following a stroke, 40% of stroke patients are left with moderate functional impairment and 15% to 30% have a severe disability as a result of a stroke. A neurogenic cognitive-communicative disorder is one result of a stroke. Neuro- meaning related to nerves or the nervous system and -genic meaning resulting from or caused by. Aphasia is one type of a neurogenic cognitive-communicative disorder which presents with impaired comprehension and production of speech and language, usually caused by damage in the language-dominant, left hemisphere of the brain. Aphasia is any disorder of language that causes the patient to have the inability to communicate, whether it is through writing, speaking, or sign language.
Brain damage
Other lesions to the visual cortex have different effects depending on the location of the damage. Lesions to V1, for example, can cause blindsight in different areas of the brain depending on the size of the lesion and location relative to the calcarine fissure. Lesions to V4 can cause color-blindness, and bilateral lesions to MT/V5 can cause the loss of the ability to perceive motion. Lesions to the parietal lobes may result in agnosia, an inability to recognize complex objects, smells, or shapes, or amorphosynthesis, a loss of perception on the opposite side of the body.
Agnosia
Speech agnosia, or auditory verbal agnosia, refers to "an inability to comprehend spoken words despite intact hearing, speech production and reading ability". Patients report that they do indeed hear sounds being produced, but that the sounds are fundamentally unrecognizable/untranslatable.Despite an inability to process what the speaker is saying, some patients have been reported to recognize certain characteristic information about the speaker's voice (such as being a man or woman).
Apperceptive agnosia
Following Hermann Munk's identification of a condition he called "Seelenblindheit" (mind-blindness) Heinrich Lissauer published an exhaustive diagnostic evaluation of a patient who could not, or only with great difficulty, visually identify common objects. Because primary visual processing was intact, Lissauer considered the possible diagnostic distinction between deficits in perception (apperceptive agnosia) and in recognition (associative agnosia).
Bulimia nervosa
Bulimics are much more likely than non-bulimics to have an affective disorder, such as depression or general anxiety disorder: A 1985 Columbia University study on female bulimics at New York State Psychiatric Institute found 70% had suffered depression some time in their lives (as opposed to 25.8% for adult females in a control sample from the general population), rising to 88% for all affective disorders combined. Another study by the Royal Children's Hospital in Melbourne on a cohort of 2,000 adolescents similarly found that those meeting at least two of the DSM-IV criteria for bulimia nervosa or anorexia nervosa had a sixfold increase in risk of anxiety and a doubled risk for substance dependency.
Some sufferers of anorexia nervosa exhibit episodes of bulimic tendencies through purging (either through self-induced vomiting or laxatives) as a way to quickly remove food in their system. There may be an increased risk for diabetes mellitus type 2. Bulimia also has negative effects on a person's teeth due to the acid passed through the mouth from frequent vomiting causing acid erosion, mainly on the posterior dental surface.
Visual agnosia
While most cases of visual agnosia are seen in older adults who have experienced extensive brain damage, there are also cases of young children with less brain damage during developmental years acquiring the symptoms. Commonly, visual agnosia presents as an inability to recognize an object in the absence of other explanations, such as blindness or partial blindness, anomia, memory loss, etc.. Other common manifestations of visual agnosia that are generally tested for include difficulty identifying objects that look similar in shape, difficulty with identifying line drawings of objects, and recognizing objects that are shown from less common views, such as a horse from a top-down view.
Auditory agnosia
Auditory agnosia is a form of agnosia that manifests itself primarily in the inability to recognize or differentiate between sounds. It is not a defect of the ear or "hearing", but rather a neurological inability of the brain to process sound meaning. It is caused by bilateral damage to the anterior superior temporal gyrus, which is part of the auditory pathway responsible for sound recognition, the auditory "what" pathway . Persons with auditory agnosia can physically hear the sounds and describe them using unrelated terms, but are unable to recognize them. They might describe the sound of some environmental sounds, such as a motor starting, as resembling a lion roaring, but would not be able to associate the sound with "car" or "engine", nor would they say that it "was" a lion creating the noise. All auditory agnosia patients read lips in order to enhance the speech comprehension. It is yet unclear whether auditory agnosia (also called general auditory agnosia) is a combination of milder disorders, such auditory verbal agnosia (pure word deafness), non-verbal auditory agnosia, amusia and word meaning deafness), or a mild case of the more severe disorder, cerebral deafness. So far, 203 patients with auditory perceptual deficits due to CNS damage were reported in the medical literature, of which 183 diagnosed with general auditory agnosia or word deafness, 34 with cerebral deafness, 51 with non-verbal auditory agnosia-amusia and 8 word meaning deafness (for a list of patients see).
Associative visual agnosia
Pure alexia ("alexia without dysgraphia" or "pure word blindness") is a category-specific agnosia, characterized by a distinct impairment in reading words, despite intact comprehension for verbally presented words, demonstrating retained semantic knowledge of words. Perceptual abilities are also intact, as assessed by word-copying tasks.
Altered state of consciousness
Cannabis is a psychoactive drug that is known to alter the state of consciousness. Cannabis alters mental activity, memory, and pain perception. One who is under the influence of cannabis may (or may not) experience degrees of paranoia, increased sensitivity, and delayed reactions not normal for their usual conscious state. A 2009 review of anxiety and cannabis studies concluded that “frequent cannabis users appear to have higher levels of anxiety than non-users,” and that “a considerable number of subjects developed anxiety disorders before the first symptoms of cannabis dependence.” That led researchers to believe that anxiety-prone people tend to use cannabis as a self-prescribed anxiety medicine, opposing the idea that cannabis is what's causing the anxiety. (Frazier, 2010)
Asemia
Asemia is the term for the medical condition of being unable to understand or express any signs or symbols.
It is a more severe condition than aphasia, which is the inability to understand linguistic signs. Asemia is caused by damage to the areas of the brain that process communication – more specifically, when there is damage to the left side of the brain in the areas that process communication such as Broca's and Wernicke's areas. Damage can be inflicted by physical trauma to the brain, but is more commonly caused by stroke and sometimes tumors. The onset of this condition is usually quick but not permanent. Treatment of this condition is traditional speech therapy in which the individual must relearn how to read, write, and talk. Depending on the severity of the injury, recovery can take days to years. Considerable recovery is common, but often not to the full extent of baseline ability.
Auditory verbal agnosia
In childhood, auditory verbal agnosia can also be caused by Landau-Kleffner syndrome, also called acquired epileptic aphasia. It is often the first symptom of this disease. A review of 45 cases suggested a relationship between prognosis and age of onset with poorer prognosis for those with earlier onset. In extremely rare cases, auditory verbal agnosia has been known to present as a symptom of neurodegenerative disease, such as Alzheimer's disease. In such cases auditory verbal agnosia is a symptom that is typically followed by more severe neurological symptoms typical of Alzheimer's disease.
Fast mapping
Fast mapping in individuals with aphasia has gained research attention due to its effect on speaking, listening, reading, and writing. Research done by Blumstein makes an important distinction between those with Broca's aphasia, who are limited in physical speech, as compared to those with Wernicke's aphasia, who cannot link words with meaning. In Broca's aphasia, Blumstein found that whereas individuals with Wernicke's aphasia performed at the same level as the normal control group, those with Broca's aphasia showed slower reaction times for word presentations after reduced voice onset time stimuli. In short, when stimuli were acoustically altered, individuals with Broca's aphasia experienced difficulty recognizing the novel stimuli upon second presentation. Bloomstein's findings reinforce the crucial difference between one's ability to retain novel stimuli versus the ability to express novel stimuli. Because individuals with Wernicke's aphasia are only limited in their understanding of semantic meaning, it makes sense that the participant's novel stimulus recall would not be affected. On the other hand, those with Broca's aphasia lack the ability to produce speech, in effect hindering their ability to recall novel stimuli. Although individuals with Broca's aphasia are limited in their speech production, it is not clear whether they simply cannot formulate the physical speech or if they actually did not process the stimuli.
Memory disorder
Alzheimer's disease (AD) is a progressive, degenerative and fatal brain disease, in which cell to cell connections in the brain are lost. Alzheimer's disease is the most common form of dementia. Globally approximately 1–5% of the population is affected by Alzheimer's disease. Women are disproportionately the victims of Alzheimer's disease, with evidence suggesting that women with AD display more severe cognitive impairment relative to age-matched males with AD, as well as a more rapid rate of cognitive decline.
Amnesia is an abnormal mental state in which memory and learning are affected out of all proportion to other cognitive functions in an otherwise alert and responsive patient. There are two forms of amnesia: Anterograde amnesia and retrograde amnesia, that show hippocampal or medial temporal lobe damage. Anterograde amnesics show difficulty in the learning and retention of information encountered after brain damage. Retrograde Amnesics generally have memories spared about personal experiences or context independent semantic information.
Glossary of psychiatry
Clouding of consciousness, also known as "brain fog" or "mental fog", is a global impairment in higher central nervous functioning. All aspects of cognitive functioning are affected. On mental status examination it is manifest by disorientation in time, place and person, memory difficulties caused by failure to register and recall, aphasia, and agnosia. Impaired perception functioning leads to illusions and hallucinations often in the visual sensory modality. This then causes agitation and distress and secondary delusions. The term 'confusion state' is sometimes used to mean clouding of consciousness, but should be avoided if at all possible because it is ambiguous.
Anosognosia
Although largely used to describe unawareness of impairment after brain injury or stroke, the term 'anosognosia' is occasionally used to describe the lack of insight shown by some people with anorexia nervosa. They do not seem to recognize that they have a mental illness. There is evidence that 'anosognosia' related to schizophrenia may be the result of frontal lobe damage. E. Fuller Torrey, a psychiatrist and schizophrenia researcher, has stated that among those with schizophrenia and bipolar disorder, anosognosia is the most prevalent reason for not taking medications.
Auditory verbal agnosia
Auditory verbal agnosia is rarely diagnosed in its pure form. Auditory verbal agnosia can both present as the result of acute damage or as chronic, progressive degeneration over time. Cases have been documented that result from severe acute head trauma resulting in bilateral temporal lobe damage. In contrast, auditory verbal agnosia has also been documented to present progressively over several years. In one such case, the patient exhibited progressive word deafness over a 9-year period but did not exhibit any other cognitive of mental deterioration. MRIs showed cortical atrophy in the left superior temporal lobe region.
Dwarfism
Mental effects also vary according to the specific underlying syndrome. In most cases of skeletal dysplasia, such as achondroplasia, mental function is not impaired. However, there are syndromes which can affect the cranial structure and growth of the brain, severely impairing mental capacity. Unless the brain is directly affected by the underlying disorder, there is little to no chance of mental impairment that can be attributed to dwarfism.
Visual agnosia
Although visual agnosia can be general, there exist many variants that impair recognition of specific types. These variants of visual agnosia include prosopagnosia (inability to recognize faces), pure word blindness (inability to recognize words, often called "agnosic alexia" or "pure alexia"), agnosias for colors (inability to differentiate colors), agnosias for the environment (inability to recognize landmarks or difficult with spatial layout of an environment, i.e. topographagnosia) and simultanagosia (inability to sort out multiple objects in a visual scene).
Anomic aphasia
Although many experts have believed that damage to Broca's area or Wernicke's area are the main causes of anomia, current studies have shown that damage in the left parietal lobe is the epicenter of anomic aphasia. One study was conducted using a word repetition test as well as fMRI in order to see the highest level of activity as well as where the lesions are in the brain tissue. Fridrikkson, et al. saw that damage to neither Broca's area nor Wernicke's area were the sole sources of anomia in the subjects. Therefore, the original anomia model, which theorized that damage occurred on the surface of the brain in the grey matter was debunked, and it was found that the damage was in the white matter deeper in the brain, on the left hemisphere. More specifically, the damage was in a part of the nerve tract called the arcuate fasciculus, for which the mechanism of action is unknown, though it is known to connect the posterior (back) of the brain to the anterior (front) and vice versa.
Amusia
Clinical symptoms of acquired amusia are much more variable than those of congenital amusia and are determined by the location and nature of the lesion. Brain injuries may afflict motor or expressive functioning, including the ability to sing, whistle, or hum a tune (oral-expressive amusia), the ability to play an instrument (instrumental amusia or musical apraxia), and the ability to write music (musical agraphia). Additionally, brain damage to the receptive dimension affects the faculty to discriminate tunes (receptive or sensorial amusia), the ability to read music (musical alessia), and the ability to identify songs that were familiar prior to the brain damage (amnesic amusia).
Associative visual agnosia
Visual object agnosia (or semantic agnosia) is the most commonly encountered form of agnosia. The clinical "definition" of the disorder is when an affected person is able to copy/draw things that they cannot recognize. Individuals afflicted with the associative type often cannot identify, describe or mimic functions of items, though perception is intact, since images of objects can be copied or drawn. Individuals may retain semantic knowledge of the items, as exemplified during tasks where objects are presented through alternate modalities, through touch or verbal naming or description. Some associative visual object agnostics retain the ability to categorize items by context or general category, though unable to name or describe them. Diffuse hypoxic damage is the most common cause of visual object agnosias.
Anomic aphasia
The best way to see if anomic aphasia has developed is by using verbal as well as imaging tests. The combination of the two tests seem to be most effective, since either test done alone may give false positives or false negatives. For example, the verbal test is used to see if there is a speech disorder, and whether it is a problem in speech production or in comprehension. Patients with Alzheimer's disease have speech problems that are linked to dementia or progressive aphasias which can include anomia. The imaging test, mostly done using MRI scans, is ideal for lesion mapping or viewing deterioration in the brain. However, imaging cannot diagnose anomia on its own because the lesions may not be located deep enough to damage the white matter or damage the arcuate fasciculus. However, anomic aphasia is very difficult to associate with a specific lesion location in the brain. Therefore, the combination of speech tests and imaging tests has the highest sensitivity and specificity.
Integrative agnosia
Integrative agnosia is a sub-disease of agnosia, meaning the lack of integrating perceptual wholes within 
knowledge. Integrative agnosia can be assessed by several experimental tests such as the Efron shape test, which 
determines the specificity of the disease being Integrative. 
This disease is often caused by brain trauma, producing medial ventral lesions to the extrastriate cortex. Affecting this region of the brain produces learning impairments: the inability to 
integrate parts such as spatial distances or producing visual images from short or long-term memory.
Anhedonia
Studies in clinical populations, healthy populations, and animal models have implicated a number of neurobiological substrates in anhedonia. Regions implicated in anhedonia include the prefrontal cortex as a whole, particularly the orbitofrontal cortex (OFC), the striatum, amygdala, anterior cingulate cortex (ACC), hypothalamus, and ventral tegmental area (VTA). Neuroimaging studies in humans have reported that deficits in consummatory aspects of reward are associated with abnormalities in the ventral striatum and medial prefrontal cortex, while deficits in anticipatory aspects of reward are related to abnormalities in hippocampal, dorsal ACC and prefrontal regions. These abnormalities are generally consistent with animal models, except for inconsistent findings with regard to the OFC. This inconsistency may be related to the difficulty in imaging the OFC due to its anatomical location, or the small number of studies performed on anhedonia; a number of studies have reported reduced activity in the OFC in schizophrenia and major depression, as well as a direct relationship between reduced activity and anhedonia.
Researchers theorize that anhedonia may result from the breakdown in the brain's reward system, involving the neurotransmitter dopamine. Anhedonia can be characterised as "impaired ability to pursue, experience and/or learn about pleasure, which is often, but not always accessible to conscious awareness".
Obstructive sleep apnea
The hypoxia (absence of oxygen supply) related to OSA may cause changes in the neurons of the hippocampus and the right frontal cortex. Research using neuro-imaging revealed evidence of hippocampal atrophy in people suffering from OSA. They found that OSA can cause problems in mentally manipulating non-verbal information, in executive functions and working memory. This repeated brain hypoxia is also considered to be a cause of Alzheimer's disease.
Agnosia
The effect of damage to the superior temporal sulcus is consistent with several types of neurolinguistic deficiencies, and some contend that agnosia is one of them. The superior temporal sulcus is vital for speech comprehension because the region is highly involved with the lexical interface. According to the 1985 TRACE II Model, the lexical interface associates sound waves (phonemes) with morphological features to produce meaningful words. This association process is accomplished by lateral inhibition/excitement of certain words within an individual's lexicon (vocabulary). For instance, if an experimenter were to say DOG aloud, the utterance would activate and inhibit various words within the subjects lexical interface:
The consistency of this model to agnosia is shown by evidence that bilateral lesions to the superior temporal sulcus produces 'pure word deafness' (Kussmaul, 1877), or as it's understood today—speech agnosia. Patients with pure word deafness demonstrate the inability to recognize and process speech sounds with normal auditory processing for non-speech sounds below the level of the cortex.
Recognition memory
Damage to the temporal lobes can also result in visual agnosia, a deficit in which patients are unable to properly recognize objects, either due to a perceptive deficit, or a deficit in semantic memory. In the process of object recognition, visual information from the occipital lobes (such as lines, movement, colour etc.) must at some point be actively interpreted by the brain and attributed meaning. This is commonly referred to in terms of the ventral, or "what" pathway, which leads to the temporal lobes. People with visual agnosia are often able to identify features of an object (it is small, cylindrical, has a handle etc.), but are unable to recognize the object as a whole (a tea cup). This has been termed specifically as integrative agnosia.
Global aphasia
Global aphasia is a severe form of nonfluent aphasia, caused by damage to the left side of the brain, that affects receptive and expressive language skills (needed for both written and oral language) as well as auditory and visual comprehension. Acquired impairments of communicative abilities are present across all language modalities, impacting language production, comprehension, and repetition. Patients with global aphasia may be able to verbalize a few short utterances and use non-word neologisms, but their overall production ability is limited. Their ability to repeat words, utterances, or phrases is also affected. Due to the preservation of the right hemisphere, an individual with global aphasia may still be able to express themselves through facial expressions, gestures, and intonation. This type of aphasia often results from a large lesion of the left perisylvian cortex. The lesion is caused by an occlusion of the left middle cerebral artery and is associated with damage to Broca's area, Wernicke's area, and insular regions which are associated with aspects of language.
Auditory agnosia
Auditory agnosia (with the exception of non-verbal auditory agnosia and amusia) is strongly dependent on damage to both hemispheres. The order of hemispheric damage is irrelevant to manifestation of symptoms, and years could take between the damage of the first hemisphere and the second hemisphere (after which the symptoms suddenly emerge). A study that compared lesion locations, reported that in all cases with bilateral hemispheric damage, at least in one side the lesion included Heschl’s gyrus or its underlying white matter. A rare insight into the etiology of this disorder was reported in a study of an auditory agnosia patient with damage to the brainstem, instead of cortex. fMRI scanning of the patient revealed weak activation of the anterior heschl's gyrus (area R) and anterior superior temporal gyrus. These brain areas are part of the auditory 'what' pathway, and are known from both human and monkey research to participate in the recognition of sounds.
Visual agnosia
Associative agnosia is an inability to identify objects even with apparent perception and knowledge of them. It involves a higher level of processing than apperceptive agnosia. Individuals with associative agnosia can copy or match simple figures, indicating that they can perceive objects correctly. They also display the knowledge of objects when tested with tactile or verbal information. However, when tested visually, they cannot name or describe common objects. This means that there is an impairment in associating the perception of objects with the stored knowledge of them.
Visual agnosia
Visual agnosia is an impairment in recognition of visually presented objects. It is not due to a deficit in vision (acuity, visual field, and scanning), language, memory, or intellect. While cortical blindness results from lesions to primary visual cortex, visual agnosia is often due to damage to more anterior cortex such as the posterior occipital and/or temporal lobe(s) in the brain. There are two types of visual agnosia: apperceptive agnosia and associative agnosia.
Auditory agnosia
In 1885, Lichtheim also reported of an auditory agnosia patient. This patient, in addition to word deafness, was impaired at recognizing environmental sounds and melodies. Based on this case study, as well as other aphasic patients, Lichtheim proposed that the language reception center receives afferents from upstream auditory and visual word recognition centers, and that damage to these regions results in word deafness or word blindness (i.e., alexia), respectively. Because the lesion of Lichtheim’s auditory agnosia patient was sub-cortical deep to the posterior STG (superior temporal gyrus), Lichtheim renamed auditory agnosia as “sub-cortical speech deafness”.
Astereognosis
Individuals with tactile agnosia may be able to identify the name, purpose, or origin of an object with their left hand but not their right, or vice versa, or both hands. Astereognosis refers specifically to those who lack tactile recognition in both hands. In the affected hand(s) they may be able to identify basic shapes such as pyramids and spheres (with abnormally high difficulty) but still not tactilely recognize common objects by easily recognizable and unique features such as a fork by its prongs (though the individual may report feeling a long, metal rod with multiple, pointy rods stemming off in uniform direction). These symptoms suggest that a very specific part of the brain is responsible for making the connections between tactile stimuli and functions/relationships of those stimuli, which, along with the relatively low impact this disorder has on a person's quality of life, helps explain the rarity of reports and research of individuals with tactile agnosia.
Social-emotional agnosia
Although rare in humans, Klüver–Bucy syndrome has many symptoms that are strikingly similar to those seen in social-emotional agnosia. The amygdala and temporal lobes have been implicated in the pathology of Klüver–Bucy syndrome as well, leading to docility, hyperorality, and in some rare cases hypersexuality. Unlike patients of social-emotional agnosia, people with Klüver–Bucy syndrome also tend to demonstrate visual agnosia (inability to recognize visual stimuli) and have difficulties with visual perception.
Global aphasia
When evaluating the prognosis of a patient, the main contributing participant factors that influence the extent of neuroplasticity, or the brain's ability to change are: age, lesion location, pre-existing cognitive status, motivation, age, overall health, and interaction amongst these. After brain damage, initial signs of global aphasia may appear within the first two days due to brain swelling (cerebral edema). With some time and natural recovery, impairment presentation may progress into expressive aphasia (most commonly) or receptive aphasia. Due to the size and location of the lesion associated with global aphasia, the prognosis for language abilities is poor. Research has shown that the prognosis of long-term language abilities is determined by the initial severity level of aphasia within the first four weeks after a stroke. As a result, there is a poor prognosis for persons who retain a diagnosis of aphasia after one month due to limited initial language abilities. Nonetheless, in the first year post-stroke, patients with global aphasia showed improvement in their Western Aphasia Battery (WAB) scores from baseline. When compared to individuals with Broca’s, Wernicke’s, anomic, and conduction types of aphasia, those with Broca’s aphasia showed the best rate and extent of improvement followed by global aphasia. The rate of improvement in language function was highest in the first four weeks after stroke.
Social-emotional agnosia
Social-emotional agnosia, also known as emotional agnosia or expressive agnosia, is the inability to perceive facial expressions, body language, and voice intonation. A person with this disorder is unable to non-verbally perceive others' emotions in social situations, limiting normal social interactions. The condition causes a functional blindness to subtle non-verbal social-emotional cues in voice, gesture, and facial expression. People with this form of agnosia have difficulty in determining and identifying the motivational and emotional significance of external social events, and may appear emotionless or agnostic (uncertainty or general indecisiveness about a particular thing). Symptoms of this agnosia can vary depending on the area of the brain affected. Social-emotional agnosia often occurs in individuals with schizophrenia and autism. It is difficult to distinguish from, and has been found to co-occur with, alexithymia.
Agnosia
In contrast, individuals with associative visual agnosia experience difficulty when asked to name objects. Associative agnosia is associated with damage to both the right and left hemispheres at the occipitotemporal border. A specific form of associative visual agnosia is known as prosopagnosia. Prosopagnosia is the inability to recognize faces. For example, these individuals have difficulty recognizing friends, family and coworkers. However, individuals with prosopagnosia can recognize all other types of visual stimuli.
Auditory verbal agnosia
Auditory verbal agnosia can be referred to as a pure aphasia because it has a high degree of specificity. Despite an inability to comprehend speech, patients with auditory verbal agnosia typically retain the ability to hear and process non-speech auditory information, speak, read and write. This specificity suggests that there is a separation between speech perception, non-speech auditory processing, and central language processing. In support of this theory, there are cases in which speech and non-speech processing impairments have responded differentially to treatment. For example, some therapies have improved writing comprehension in patients over time, while speech remained critically impaired in those same patients.
Fusiform body area
There is evidence that the FBA plays a critical role in how individuals with Anorexia Nervosa (AN) perceive their own bodies and the bodies of others. In the article Body Image Distortion Reveals Amygdala Activation in Patients with Anorexia Nervosa - a Functional Magnetic Resonance Imaging Study" by Gert Seeger and colleagues found that as well as amygdala activation (the brain's fear network), there was activation in the right gyrus fusiform in anorectic patients, but not healthy age-matched controls. This suggests that due to being overly aware and critical of body forms, increased activation in what we now know as the FBA is to be expected. As this study was conducted before the identification of the FBA, the fusiform gyrus activation can be considered previous evidence for the FBA being involved in body perception.
Opioid overdose
Permanent brain damage may occur due to cerebral hypoxia or opioid-induced neurotoxicity. Opioids inhibit the medulla's chemoreceptors through the mu and delta receptors. Opioids bind to receptors that are part of the endogenous opioid system as well as other central nervous neurotransmitter systems, binding to excitatory neurotransmitters like dopamine or glutamate, or inhibitory neurotransmitters like GABA. The main excitatory chemoreceptor, glutamate, and main inhibitory chemoreceptor, GABA, are the main neurotransmitters that control respiration. Because of its fatal consequences, opioid induced respiratory depression is one of the major limiting factors of its analgesic effects. Opioids vary in the rate of metabolism amongst individuals. The rate of metabolism of opiates vary due to genetic factors while tolerance of the opiates can determine risk.
Apperceptive agnosia
Visual agnosia (both apperceptive and associative) is prevalent in Alzheimer’s Disease (AD) patients. Visual agnosia may be present in early stages of AD and can often act as an indicator of AD. Apperceptive agnosia results from diffuse cortical pathology of AD. There is early involvement in the hippocampus and the entorhinal cortex followed by a spread to adjacent areas with neurofibrillary tangles (NFT). Gradual extension of NFT throughout the occipital, parietal, and temporal regions devoted to vision occur resulting in visual agnosia.
Cognitive disorder
Although Alzheimer's disease accounts for the majority of cases of neurocognitive disorders, there are various medical conditions that affect mental functions such as memory, thinking, and the ability to reason, including frontotemporal degeneration, Huntington’s disease, Lewy body disease, traumatic brain injury (TBI), Parkinson’s disease, prion disease, and dementia/neurocognitive issues due to HIV infection.
Neurocognitive disorders are diagnosed as mild and major based on the severity of their symptoms. While anxiety disorders, mood disorders, and psychotic disorders can also have an effect on cognitive and memory functions, the DSM-IV-TR does not consider these cognitive disorders, because loss of cognitive function is not the primary (causal) symptom. Additionally, developmental disorders such as Autism spectrum disorder are typically developed at birth or early in life as opposed to the acquired nature of neurocognitive disorders.
Hyperkinesia
Since the basal ganglia often have many connections with the frontal lobe of the brain, hyperkinesia can be associated with neurobehavioral or neuropsychiatric disorders such as mood changes, psychosis, anxiety, disinhibition, cognitive impairments, and inappropriate behavior.
Anorexia nervosa (differential diagnoses)
The differential diagnoses of anorexia nervosa (AN) includes various types of medical and psychological conditions, which may be misdiagnosed as AN. In some cases, these conditions may be comorbid with AN because the misdiagnosis of AN is not uncommon. For example, a case of achalasia was misdiagnosed as AN and the patient spent two months confined to a psychiatric hospital. A reason for the differential diagnoses that surround AN arise mainly because, like other disorders, it is primarily, albeit defensively and adaptive for, the individual concerned. 
Anorexia Nervosa is a psychological disorder characterized by extremely reduced intake of food. People suffering from Aneroxia Nervosa have a low self-image and consider themselves overweight.
Common behaviors and signs of someone suffering from AN:Some of the differential or comorbid medical diagnoses may include:
Anosognosia
Anosognosia can be selective in that an affected person with multiple impairments may seem unaware of only one handicap, while appearing to be fully aware of any others. This is consistent with the idea that the source of the problem relates to spatial representation of the body. For example, anosognosia for hemiplegia, or the paralysis of one side of the body, may occur with or without intact awareness of visuo-spatial unilateral neglect. This phenomenon of double dissociation can be an indicator of domain-specific disorders of awareness modules, meaning that in anosognosia, brain damage can selectively impact the self-monitoring process of one specific physical or cognitive function rather than a spatial location of the body.
Alcohol withdrawal syndrome
Binge drinking is associated with increased impulsivity, impairments in spatial working memory and impaired emotional learning. These adverse effects are believed to be due to the neurotoxic effects of repeated withdrawal from alcohol on aberrant neuronal plasticity and cortical damage. Repeated periods of acute intoxication followed by acute detoxification has profound effects on the brain and is associated with an increased risk of seizures as well as cognitive deficits. The effects on the brain are similar to those seen in alcoholics who have been detoxified repeatedly but not as severe as in alcoholics who have no history of prior detox. Thus the acute withdrawal syndrome appears to be the most important factor in causing damage or impairment to brain function. The brain regions most sensitive to harm from binge drinking are the amygdala and prefrontal cortex.
Neurotoxin
Ammonia toxicity is often seen through two routes of administration, either through consumption or through endogenous ailments such as liver failure. One notable case in which ammonia toxicity is common is in response to cirrhosis of the liver which results in hepatic encephalopathy, and can result in cerebral edema (Haussinger 2006). This cerebral edema can be the result of nervous cell remodeling. As a consequence of increased concentrations, ammonia activity in-vivo has been shown to induce swelling of astrocytes in the brain through increased production of cGMP (Cyclic Guanosine Monophosphate) within the cells which leads to Protein Kinase G-mediated (PKG) cytoskeletal modifications. The resultant effect of this toxicity can be reduced brain energy metabolism and function. Importantly, the toxic effects of ammonia on astrocyte remodling can be reduced through administration of L-carnitine. This astrocyte remodeling appears to be mediated through ammonia-induced mitochondrial permeability transition. This mitochondrial transition is a direct result of glutamine activity a compound which forms from ammonia in-vivo. Administration of antioxidants or glutaminase inhibitor can reduce this mitochondrial transition, and potentially also astrocyte remodeling.
Visual agnosia
Within any given patient, a variety of symptoms can occur, and the impairment of ability is not only binary but can range in severity. For example, Patient SM is a prosopagnosic with a unilateral lesion to left extrastriate cortex due to an accident in his twenties who displays behavior similar to congenital prosopagnosia. Although he can recognize facial features and emotions – indeed he sometimes uses a standout feature to recognize a face – face recognition is almost impossible purely from visual stimuli, even for faces of friends, family, and himself. The disorder also affects his memory of faces, both in storing new memories of faces and recalling stored memories.
Auditory agnosia
Auerbach et al considered word deafness and general auditory agnosia as two separate disorders, and labelled general auditory agnosia as pre-phonemic auditory agnosia and word deafness as post-phonemic auditory agnosia. They suggested that pre-phonemic auditory agnosia manifests because of general damage to the auditory cortex of both hemispheres, and that post-phonemic auditory agnosia manifests because of damage to a spoken word recognition center in the left hemisphere. Recent evidence, possibly verified Auerbach hypothesis, since an epileptic patient who undergone electro-stimulation to the anterior superior temporal gyrus was demonstrated a transient loss of speech comprehension, but with intact perception of environmental sounds and music.
Psychosis
NMDA receptor dysfunction has been proposed as a mechanism in psychosis. This theory is reinforced by the fact that dissociative NMDA receptor antagonists such as ketamine, PCP and dextromethorphan (at large overdoses) induce a psychotic state. The symptoms of dissociative intoxication are also considered to mirror the symptoms of schizophrenia, including negative psychotic symptoms. NMDA receptor antagonism, in addition to producing symptoms reminiscent of psychosis, mimics the neurophysiological aspects, such as reduction in the amplitude of P50, P300, and MMN evoked potentials. Hierarchical Bayesian neurocomputational models of sensory feedback, in agreement with neuroimaging literature, link NMDA receptor hypofunction to delusional or hallucinatory symptoms via proposing a failure of NMDA mediated top down predictions to adequately cancel out enhanced bottom up AMPA mediated predictions errors. Excessive prediction errors in response to stimuli that would normally not produce such as response is thought to confer excessive salience to otherwise mundane events. Dsyfunction higher up in the hierarchy, where representation is more abstract, could result in delusions. The common finding of reduced GAD67 expression in psychotic disorders may explain enhanced AMPA mediated signaling, caused by reduced GABAergic inhibition.
Cognitive flexibility
Diminished cognitive flexibility has been noted in a variety of neuropsychiatric disorders such as anorexia nervosa, obsessive–compulsive disorder, schizophrenia, autism, and in a subset of people with ADHD. Each of these disorders exhibit varying aspects of cognitive inflexibility. For example, those with obsessive–compulsive disorder experience difficulty shifting their attentional focus as well as inhibiting motor responses. Children with autism show a slightly different profile with deficits in adjusting to changing task contingencies, while often maintaining the ability to respond in the face of competing responses. Potential treatments may lie in neurochemical modulation. Juveniles with Anorexia nervosa have marked decreases in set-shifting abilities, possibly associated with incomplete maturation of prefrontal cortices associated with malnutrition. One can also consider people with addictions to be limited in cognitive flexibility, in that they are unable to flexibly respond to stimuli previously associated with the drug.
Neural processing for individual categories of objects
Studies of patients with brain damage have revealed pure agnosic disorders that selectively impair recognition of specific object categories. Such agnosic disorders have been reported for faces (prosopagnosia), living vs. nonliving stimuli, fruits, vegetables, tools, and musical instruments among others, suggesting that such categories may be processed independently within the brain.