Central facial palsy (colloquially referred to as central seven) is a symptom or finding characterized by paralysis or paresis of the lower half of one side of the face. It usually results from damage to upper motor neurons of the facial nerve.

The facial motor nucleus has dorsal and ventral divisions that contain lower motor neurons supplying the muscles of the upper and lower face, respectively. The dorsal division receives upper motor neuron input (i.e. from both sides of the brain) while the ventral division receives only contralateral input (i.e. from the opposite side of the brain).

Thus, lesions of the corticobulbar tract between the cerebral cortex and pons and the facial motor nucleus destroy or reduce input to the ventral division, but ipsilateral input (i.e. from the same side) to the dorsal division is retained. As a result, central facial palsy is characterized by hemiparalysis or hemiparesis of the contralateral muscles of facial expression, but not the muscles of the forehead.

Even though the causes of dysosmia are not yet clear, there are two general theories that describe the etiology: the peripheral and central theories. In parosmia, the peripheral theory refers to the inability to form a complete picture of an odorant due to the loss of functioning olfactory receptor neurons. The central theory refers to integrative centers in the brain forming a distorted odor. In phantosmia, the peripheral theory refers to neurons emitting abnormal signals to the brain or the loss of inhibitory cells that are normally present in normal functioning. The central theory for phantosmia is described as an area of hyper-functioning brain cells that generate the order perception. Evidence to support these theories include findings that for the majority of individuals with distortions, there is a loss of sensitivity to smell that accompanies it and the distortions are worse at the time of the decreased sensitivity. It has been reported in parosmia cases that patients can identify triggering stimuli. Common triggers include gasoline, tobacco, coffee, perfum, fruits and chocolate.

The cause of dysosmia has not been determined but there have been clinical associations with the neurological disorder:

- Upper respiratory tract infection (URTIs)

- Nasal and paranasal sinus disease

- Toxic chemical exposure

- Neurological abnormalities

- Head trauma

- Nasal surgery

- Tumors on the frontal lobe or olfactory bulb

- Epilepsy

Most of cases are described as idiopathic and the main antecedents related to parosmia are URTIs, head trauma, and nasal and paranasal sinus disease. Psychiatric causes for smell distortion can exist in schizophrenia, alcoholic psychosis, depression, and olfactory reference syndrome.

The frequency of phantosmia is rare in comparison with the frequency of parosmia. Parosmia has been estimated to be in 10-60% of patients with olfactory dysfunction and from studies, it has been shown that it can last anywhere from 3 months to 22 years. Smell and taste problems result in over 200,000 visits to physicians annually in the US. Lately, it has been thought that phantosmia might co-occur with Parkinson's disease. However, its potential to be a premotor biomarker for Parkinson's is still up for debate as not all patients with Parkinson's disease have olfactory disorders

Of the millions experiencing strokes worldwide, over 30,000 in the United States alone have developed some form of Dejerine–Roussy syndrome. 8% of all stroke patients will experience central pain syndrome, with 5% experiencing moderate to severe pain. The risk of developing Dejerine–Roussy syndrome is higher in older stroke patients, about 11% of stroke patients over the age of 80.

Studies have shown that PCA may be a variant of Alzheimer's disease (AD), with an emphasis on visual deficits. Although in primarily different, but sometimes overlapping, brain regions, both involve progressive neural degeneration, as shown by the loss of neurons and synapses, and the presence of neurofibrillary tangles and senile plaques in affected brain regions; this eventually leads to dementia in both diseases. PCA patients have more cortical damage and gray matter (cell body) loss in posterior regions, especially in the occipital, parietal, and temporal lobes, whereas Alzheimer’s patients typically experience more damage in the prefrontal cortex and hippocampus. PCA tends to impair working memory and anterograde memory, while leaving episodic memory intact, whereas AD patients typically have damaged episodic memory, suggesting some differences still lie in the primary areas of cortical damage.

Over time, however, atrophy in PCA patients may spread to regions commonly damaged in AD patients, leading to common AD symptoms such as deficits in memory, language, learning, and cognition. Although PCA has an earlier onset, many PCA patients have also been diagnosed with Alzheimer’s, suggesting that the degeneration has simply migrated anteriorly to other cortical brain regions.

There is no standard definition of PCA and no established diagnostic criteria, so it is not possible to know how many people have the condition. Some studies have found that about 5 percent of people diagnosed with Alzheimer’s disease have PCA. However, because PCA often goes unrecognized, the true percentage may be as high as 15 percent. Researchers and physicians are working to establish a standard definition and diagnostic criteria for PCA.

PCA may also be correlated with the diseases of Lewy body, Creutzfeldt–Jakob disease, Bálint's syndrome, and Gerstmann syndrome. In addition, PCA may result in part from mutations in the presenilin 1 gene (PSEN1).

Although there are many contributing factors and risks associated with strokes, there are very few associated with Dejerine–Roussy syndrome and thalamic lesions specifically. In general, strokes damage one hemisphere of the brain, which can include the thalamus. The thalamus is generally believed to relay sensory information between a variety of subcortical areas and the cerebral cortex. It is known that sensory information from environmental stimuli travels to the thalamus for processing and then to the somatosensory cortex for interpretation. The final product of this communication is the ability to see, hear or feel something as interpreted by the brain. Dejerine–Roussy syndrome most often compromises tactile sensation. Therefore, the damage in the thalamus causes miscommunication between the afferent pathway and the cortex of the brain, changing what or how one feels. The change could be an incorrect sensation experienced, or inappropriate amplification or dulling of a sensation. Because the brain is considered plastic and each individual's brain is different, it is almost impossible to know how a sensation will be changed without brain mapping and individual consultation.

Recently, magnetic resonance imaging has been utilized to correlate lesion size and location with area affected and severity of condition. Although preliminary, these findings hold promise for an objective way to understand and treat patients with Dejerine–Roussy syndrome.

Clinical presentation of CBD usually does not occur until age 60, with the earliest recorded diagnosis and subsequent postmortem verification being age 28. Although men and women present with the disease, some analysis has shown a predominant appearance of CBD in women. Current calculations suggest that the prevalence of CBD is approximately 4.9 to 7.3 per 100,000 people. The prognosis for an individual diagnosed with CBD is death within approximately eight years, although some patients have been diagnosed over 17 years ago (2017) and are still in relatively good standing, but with serious debilitation such as dysphagia, and overall limb rigidity. The partial (or total) use of a feeding tube may be necessary and will help prevent aspiration pneumonia, primary cause of death in CBD. Incontinence is common, as patients often can't express their need to go, due to eventual loss of speech. Therefore, proper hygiene is mandatory to prevent urinary tract infections.

Blocq's disease was first considered by Paul Blocq (1860–1896), who described this phenomenon as the loss of memory of specialized movements causing the inability to maintain an upright posture, despite normal function of the legs in the bed. The patient is able to stand up, but as soon as the feet are on the ground, the patient cannot hold himself upright nor walk; however when lying down, the subject conserved the integrity of muscular force and the precision of movements of the lower limbs. The motivation of this study came when a fellow student Georges Marinesco (1864) and Paul published a case of parkinsonian tremor (1893) due to a tumor located in the substantia nigra.

In the third paper published by Paul Blocq, he was trying to determine the neurophysiology behind this disease by relating the cerebral cortex (the decision making) and the spinal cord (the decision executer). His hypothesis was that there would exist an inhibitory influence which exerted and influenced the cortical or spinal centers for standing and walking.

Posterior cortical atrophy (PCA), also called Benson's syndrome, is a form of dementia which is usually considered an atypical variant of Alzheimer's disease (AD). The disease causes atrophy of the posterior part of the cerebral cortex, resulting in the progressive disruption of complex visual processing. PCA was first described by D. Frank Benson in 1988.

In rare cases, PCA can be caused by dementia with Lewy bodies and Creutzfeldt–Jakob disease.

PCA usually affects people at an earlier age than typical cases of Alzheimer's disease, with initial symptoms often experienced in people in their mid-fifties or early sixties. This was the case with writer Terry Pratchett (1948-2015), who went public in 2007 about being diagnosed with PCA. In "The Mind's Eye", neurologist Oliver Sacks examines the case of concert pianist Lilian Kallir (1931–2004), who suffered from PCA.

There has not been extensive research into environmental causes of hyperosmia, but there are some theories of some possible causes.

In a study by Atianjoh et al., it has been found that amphetamines decrease levels of dopamine in the olfactory bulbs of rodents. On this basis, it has been hypothesized that amphetamine use may cause hyperosmia in rodents and humans, but further research is still needed. Anecdotal support for the belief that amphetamines may cause hyperosmia comes from Oliver Sacks's account of a patient with a heightened sense of smell after taking amphetamines.

It has been observed that the inhalation of hydrocarbons can cause hyperosmia, most likely due to the destruction of dopaminergic neurons in the olfactory bulb.

Methotrexate, administered in the treatment of psoriasis, has been known to cause hyperosmia, and may be more likely to do so in patients with a history of migraines. However, this is only an observation and not part of a study, therefore it is yet to be verified.

There is physiological intracranial calcification in about 0,3-1,5% of individuals. Fahr's disease is a rare, genetically dominant, inherited neurological disorder characterized by abnormal deposits of calcium, primarily in the basal ganglia.

PANDAS is a hypothesis that there exists a subset of children with rapid onset of obsessive-compulsive disorder (OCD) or tic disorders and these symptoms are caused by group A beta-hemolytic streptococcal (GABHS) infections. The proposed link between infection and these disorders is that an initial autoimmune reaction to a GABHS infection produces antibodies that interfere with basal ganglia function, causing symptom exacerbations. It has been proposed that this autoimmune response can result in a broad range of neuropsychiatric symptoms.

Status marmoratus is a congenital condition due to maldevelopment of the corpus striatum associated with choreoathetosis, in which the striate nuclei have a marble-like appearance caused by altered myelination in the putamen, caudate, and thalamus(there is bilateral hyperdensities restricted to thalamus ). This causes lesions resulting from acute total asphyxia in the basal nucleus of full-term infants. Associated with athetoid cerebral palsy.

Normal olfactory acuity will usually return over time if the cause is environmental, even if it is untreated. The hyperosmic person may need to be removed from strong odorants for a period of time if the sensation becomes unbearable. Before they had been discontinued due to undesirable side effects, butyrophenones or thioridazine hydrochloride, both of which are dopamine antagonists, have been used to treat hyperosmia.

Parinaud's Syndrome results from injury, either direct or compressive, to the dorsal midbrain. Specifically, compression or ischemic damage of the mesencephalic tectum, including the superior colliculus adjacent oculomotor (origin of cranial nerve III) and Edinger-Westphal nuclei, causing dysfunction to the motor function of the eye.

Classically, it has been associated with three major groups:

1. Young patients with brain tumors in the pineal gland or midbrain: pinealoma (intracranial germinomas) are the most common lesion producing this syndrome.

2. Women in their 20s-30s with multiple sclerosis

3. Older patients following stroke of the upper brainstem

However, any other compression, ischemia or damage to this region can produce these phenomena: obstructive hydrocephalus, midbrain hemorrhage, cerebral arteriovenous malformation, trauma and brainstem toxoplasmosis infection. Neoplasms and giant aneurysms of the posterior fossa have also been associated with the midbrain syndrome.

Vertical supranuclear ophthalmoplegia has also been associated with metabolic disorders, such as Niemann-Pick disease, Wilson's disease, kernicterus, and barbiturate overdose.

Athetosis is a commonly occurring symptom in the disease cerebral palsy. Of all people with the disease, between 16% and 25% of them actually exhibit the symptom of athetosis. A component of this is the finding that most often the symptoms that involve athetosis occur as a part of choreoathetosis as opposed to athetosis alone.

It is also noteworthy that the presence of athetosis in cerebral palsy (as well as other conditions) causes a significant increase in a person’s basal resting metabolic rate. It has been observed that those who have cerebral palsy with athetosis require approximately 500 more Calories per day than their non-cerebral palsy non-athetoid counterpart.

Parinaud's syndrome, also known as dorsal midbrain syndrome, vertical gaze palsy, and Sunset Sign, is an inability to move the eyes up and down. It is caused by compression of the vertical gaze center at the rostral interstitial nucleus of medial longitudinal fasciculus (riMLF). The eyes lose the ability to move upward and down .

It is a group of abnormalities of eye movement and pupil dysfunction. It is caused by lesions of the upper brain stem and is named for Henri Parinaud (1844–1905), considered to be the father of French ophthalmology.

Chorea is another condition which results from damage to the basal ganglia. Similar to athetosis, it results from mutations affecting the pallidum inhibition of the thalamus as well as increased dopaminergic activity at the level of the striatum. Considering the etiology of both disorders are fairly similar, it comes as no surprise that chorea and athetosis can and usually do occur together in a condition called choreoathetosis.

Brown-Séquard syndrome is rare as the trauma would have to be something that damaged the nerve fibres on just one half of the spinal cord.

A lack of motivation has been reported in 25–50% of patients with Alzheimer's disease. While depression is also common in patients with this disease, aboulia is not a mere symptom of depressions because more than half of the patients with Alzheimer's disease with aboulia do not suffer from depression. Several studies have shown that aboulia is most prevalent in cases of severe dementia which may result from reduced metabolic activity in the prefrontal regions of the brain. Patients with Alzheimer's disease and aboulia are significantly older than patients with Alzheimer's who do not lack motivation. Going along with that, the prevalence of aboulia increased from 14% in patients with a mild case Alzheimer's disease to 61% in patients with a severe case of Alzheimer's disease, which most likely developed over time as the patient got older.

From the knowledge of the sensimotor development a number of other automatic reactions were distinguished, such as balance, support and automatic adaptations of muscle power changes to postures. Patients with hemiplegia have movements that are lower level and less motor coordination, and often must relearn these movements to continue or gain normal automatic transitions in the body. Neuro developmental treatment (NDT) often improves daily functioning and self-help. This treatment centers on reversing disabilities, specifically for patients who are hemiplegic with impaired sensimotor and neuropsychological functions. Muscle regulation that is disturbed, often called hypo or hypertonic, causes abnormal movement patterns. These automatic reactions are impaired, and patients must learn these movements and remember mentally and physically the positions.

NDT uses muscle power techniques through inhibiting and stimulating certain muscle groups, which aims to lower or increase muscle tone. For facial expression, therapists often help the patient make facial expressions by manipulating specific muscles with their fingers. The patient then tries to imitate the facial expressions. Speech therapy helps correct word pronunciation. NDT is directed at the functioning of the whole body, and not just the face. Understanding the direct mechanisms of the face is required to determine the dysfunction of specific muscles. NDT seems to be effective, but spontaneous motor movement that is controlled was not examined.

Many different causes of aboulia have been suggested. While there is some debate about the validity of aboulia as a separate disease, experts mostly agree that aboulia is the result of frontal lesions and not with cerebellar or brainstem lesions. As a result of more and more evidence showing that the mesolimbic and the mesocortical dopamine system are key to motivation and responsiveness to reward, aboulia may be a dopamine-related dysfunction. Aboulia may also result from a variety of brain injuries which cause personality change, such as dementing illnesses, trauma, or intracerebral hemorrhage (stroke), especially stroke causing diffuse injury to the right hemisphere.

Simultanagnosia (or simultagnosia) is a rare neurological disorder characterized by the inability of an individual to perceive more than a single object at a time. This type of visual attention problem is one of three major components (the others being optic ataxia and optic apraxia) of Bálint's syndrome, an uncommon and incompletely understood variety of severe neuropsychological impairments involving space representation (visuospatial processing). The term "simultanagnosia" was first coined in 1924 by Wolpert to describe a condition where the affected individual could see individual details of a complex scene but failed to grasp the overall meaning of the image.

Simultanagnosia can be divided into two different categories: dorsal and ventral. Ventral occipito-temporal lesions cause a mild form of the disorder, while dorsal occipito-parietal lesions cause a more severe form of the disorder.

Constructional apraxia is characterized by an inability or difficulty to build, assemble, or draw objects. Apraxia is a neurological disorder in which people are unable to perform tasks or movements even though they understand the task, are willing to complete it, and have the physical ability to perform the movements. Constructional apraxia may be caused by lesions in the parietal lobe following stroke or it may serve as an indicator for Alzheimer's disease.

A key deficit in constructional apraxia patients is the inability to correctly copy or draw an image. There are qualitative differences between patients with left hemisphere damage, right hemisphere damage, and Alzheimer's Disease.