Physiology of CNS Sensory Receptors

Sensory receptors respond to a specific type of stimulus, like heat or pressure. This means they're specialized for detecting only their specific modality.

A receptor potential is a graded potential that occurs when a sensory receptor is stimulated by its specific stimulus. It's a temporary change in the receptor's membrane potential.

Receptor potentials can summate over time (temporal summation) or across space (spatial summation), just like other graded potentials.

Rapidly adapting receptors respond strongly to a change in stimulus but quickly decrease their firing rate even if the stimulus remains constant. They detect changes in stimulus, not its duration.

Slowly adapting receptors maintain a constant rate of firing as long as the stimulus is present. They signal the duration of the stimulus.

Sensory receptors follow the law of specific nerve energies, which means that each sensory receptor is specific for a single type of stimulus. The brain interprets the signals based on the type of receptor that is activated.

Adaptation is the gradual decrease in the firing rate of a sensory receptor despite a constant stimulus. It allows the nervous system to focus on changes in the environment, not constant background stimuli.

Phasic receptors are rapidly adapting receptors. They are sensitive to changes in stimulus intensity and are important for detecting movement and changes in the environment.

The change in membrane potential of a sensory receptor when it's stimulated by its specific stimulus. It's graded, meaning its magnitude varies with the stimulus strength.

While it can be graded, it doesn't follow the all-or-none law. It can be summated, meaning multiple signals can add up to create a stronger response.

They're found in muscles, tendons, and ligaments. They are responsible for providing information about body position and movement.

They keep firing signals as long as the stimulus is present. They're good for detecting constant stimuli, like body position or blood pressure.

They have a rapid initial response but quickly decrease their firing rate even if the stimulus remains constant. They detect changes in stimulus, not its duration.

The brain understands the type of stimulus based on which specific sensory neuron is activated. Each neuron is specialized for a particular type of stimulus.

Receptor potential strength increases as the stimulus intensity increases. This tells the brain how strong the stimulus is.

The way the sensory neuron is connected to the brain determines where the stimulus is perceived. This is why touching different parts of your skin feels different.

A part of the cerebellum located in the midline, crucial for coordinating movements and posture.

Emotional disturbances, particularly flattening of affect or disinhibition, may arise from lesions in the limbic cerebellum, which is connected to brain regions associated with emotions.

Disruptions in the communication pathway between the posterior cerebellar lobe and cerebral association areas can negatively impact cognitive abilities like multitasking and planning.

Agrammatism, a speech deficit characterized by difficulty in constructing grammatically correct sentences, is commonly observed in individuals with Cerebellar Cognitive Affective Syndrome (CCAS).

The symptoms of Cerebellar Cognitive Affective Syndrome (CCAS) are linked to disruptions in the connections between the cerebellum and various brain regions, including limbic circuitry and cortical areas.

Recent research suggests that cerebellar gray matter, which is crucial for motor control and coordination, undergoes significant volumetric reductions in various regions of the brain in individuals with Alzheimer's disease (AD).

Studies have shown that significant atrophy (shrinkage) occurs in specific regions of the cerebellum, including the anterior lobe and lobule VI, in patients with Alzheimer's disease (AD).

Amyloid-beta (Aβ) deposits, a hallmark of Alzheimer's disease, are more prevalent in late-onset Alzheimer's disease compared to early-onset Alzheimer's disease.

Obstruction of the venous system can significantly increase intracranial pressure (ICP). This is because the venous system is responsible for draining blood from the brain, and obstruction prevents normal drainage.

The rapid venous drainage from circumventricular organs is crucial for regulating the composition of cerebrospinal fluid (CSF). These organs have a unique blood supply and filter blood to maintain the CSF's chemical balance.

The foramina of Luschka and Magendie are openings that allow CSF to flow from the fourth ventricle into the subarachnoid space. This path is essential for circulating CSF around the brain and spinal cord.

Arachnoid granulations act as one-way valves, allowing CSF to flow from the subarachnoid space into the dural venous sinuses. This mechanism ensures that CSF is reabsorbed back into the bloodstream.

The pressure gradient between CSF and venous blood drives the movement of CSF into the dural venous sinuses. When CSF pressure is higher, it pushes CSF into the sinuses where blood pressure is lower.

Disruptions in CSF reabsorption can lead to hydrocephalus, a condition where there is an excessive buildup of CSF in the brain. This can cause pressure on brain tissue, leading to various neurological symptoms.

CSF analysis is important in neurology to diagnose various conditions, such as infections, inflammation, and bleeding in the brain. It provides valuable information about the health of the central nervous system.

When cerebrospinal fluid pressure increases, arachnoid villi disengage from the dural sinuses, preventing further CSF flow. This adaptive mechanism helps to regulate CSF pressure and prevent damage to the brain.

Patients with bulimia nervosa (BN) show increased brain activity in the lateral prefrontal cortex when exposed to food cues.

Patients with anorexia nervosa (AN) exhibit lower brain activity in the lateral prefrontal cortex when exposed to food cues.

AN patients who did not reach a healthy weight at the end of treatment had a smaller right cerebellar crus I volume at the beginning of treatment.

Eating disorders, compared to healthy individuals, generally exhibit less connectivity between the insula and vermis.

Andreasen's hypothesis suggests cerebellar dysfunction, particularly in cerebello-thalamo-cortical circuits, is a fundamental aspect of schizophrenia.

Dysmetria, a lack of coordination, is a type of symptom associated with cerebellar dysfunction in schizophrenia.

Andreasen believed that schizophrenia is caused by a dysfunction of the cerebello-thalamo-cortical pathways.

Reduced volume of the cerebellum, including the cerebellar vermis, has been consistently observed in patients with schizophrenia.

Changes in cerebellar volume in schizophrenia are associated with neural and behavioral abnormalities occuring during prenatal development and other factors.

Functional imaging reveals decreased blood flow to the cerebellum, both the cortex and the vermis, in schizophrenia patients during cognitive tasks.

The cerebellum is involved in the neural circuitry of fear and anxiety-related areas and is connected to regions responsible for these emotions.

In patients with specific phobias, cerebellar activation increases in correlation with the level of anxiety caused by viewing feared stimuli. The more fear, the more active the cerebellum.

Successful cognitive-behavioral therapy (CBT) in patients with panic disorder leads to a decrease in the enhanced cerebellar activity observed before treatment.

In patients with schizophrenia, impairments in eyeblink conditioning, abnormal posture and proprioception, enhanced sensory processing, and dyscoordination of sensorimotor processes are common.

Impairments in eyeblink conditioning, abnormal posture and proprioception, enhanced sensory processing, and dyscoordination of sensorimotor processes are often observed in patients with schizophrenia.