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The ability to understand language and produce speech is associated with several areas of the cerebral cortex. Basically, spoken language is first perceived in the auditory cortex, while written text, or sign language, is processed in the visual cortex. This information is then sent to the Wernicke’s area, in the temporal lobe, where it is matched against the person’s vocabulary stored in the memory. This is where meaning is assigned to words and language comprehension is achieved.  The signals are then transmitted via a bundle of nerve fibers, known as the arcuate fasciculus, to Broca’s area in the frontal lobe.  Broca’s area is responsible for production of speech. Output from Broca’s area goes to the motor cortex which controls muscle movements necessary for speech.

A language disorder caused by brain damage is called aphasia. Lesions in the Wernicke’s area cause sensory, or receptive, aphasia. Wernicke’s aphasics have trouble understanding language, whether it is spoken or written, but have NO motor problems. They can speak at a fluent pace but their speech is often INcoherent. It can be described as a strange mixture of words that may sound like complete sentences but makes no sense and has nothing to do with the subject of conversation.

Patients with lesions in the Broca’s area, on the other hand, CAN understand language, but have difficulties speaking. They talk slowly, searching for words, forming INcomplete sentences with poor syntax, but usually manage to say important words to get their message across.

In the early days, research of language pathways was based mainly on studying patients who had a specific language deficit that could be associated with a specific brain damage. Nowadays, advanced brain imaging techniques allow mapping, in real time, the areas of the brain that are activated when a person carries on a specific task. Thanks to these techniques, a THIRD area is found to be essential for language comprehension: the inferior parietal lobule. This lobule is not only connected to both Wernicke’s and Broca’s, but also to the auditory, visual, and somatosensory cortical areas. The inferior parietal lobule is therefore perfectly wired to perform a multimodal, complex synthesis of information; it can process and connect different word elements such as the sound of the word with the look and feel of the object.

The languages centers are usually located in ONLY ONE hemisphere – the “dominant” hemisphere of the brain, which is the LEFT side in RIGHT-handed people. The corresponding areas in the right hemisphere are responsible for the emotional aspect of language. Lesions in the right hemisphere do NOT affect speech comprehension or formation but result in emotionless speech and inability to understand the emotion behind the speech such as sarcasm or a joke.  The right hemisphere may also develop to take over the MAIN language functions if the left side is damaged in early childhood. This phenomenon is known as neuroplasticity.

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The autonomic nervous system, or ANS, is the part of the nervous system that regulates activities of internal organs. The ANS is largely AUTONOMOUS, acting independently of the body’s consciousness and voluntary control. It has two main divisions: sympathetic, SNS, and parasympathetic, PSNS.

In situations that require alertness and energy, such as facing danger or doing physical activities, the ANS activates its sympathetic division to mobilize the body for action. This division increases cardiac output, accelerates respiratory rate, releases stored energy, and dilates pupils. At the same time, it also inhibits body processes that are less important in emergencies, such as digestion and urination.

On the other hand, during ordinary situations, the parasympathetic division conserves and restores. It slows heartbeats, decreases respiratory rate, stimulates digestion, removes waste and stores energy.

The sympathetic division is therefore known as the “fight or flight” response, while the parasympathetic division is associated with the “rest and digest” state.

Despite having opposite effects on the same organ, the SNS and PSNS are NOT mutually exclusive. In most organs, both systems are simultaneously active, producing a background rate of activity called the “autonomic tone” – a balance between sympathetic and parasympathetic inputs. This balance SHIFTS, one way or the other, in response to the body’s changing needs.

Some organs, however, receive inputs from ONLY ONE system. For example, the smooth muscles of blood vessels only receive sympathetic fibers, which keep them partially constricted and thus maintaining normal blood pressure. An increase in sympathetic firing rate causes further constriction and increases blood pressure, while a decrease in firing rate dilates blood vessels, lowering blood pressure.

The autonomic nerve pathways, from the control centers in the central nervous system to the target organs, are composed of 2 neurons, which meet and synapse in an autonomic ganglion. Accordingly, these neurons are called preganglionic and postganglionic.

In the SNS, the preganglionic neurons arise from the thoracic and lumbar regions of the spinal cord; their fibers exit by way of spinal nerves to the nearby sympathetic chain of ganglia. Once in the chain, preganglionic fibers may follow any of 3 routes: some fibers synapse immediately with postganglionic neurons; some travel up or down the chain before synapsing; some pass through the chain without synapsing – this third group continues as splanchnic nerves to nearby collateral ganglia for synapsing instead. From the ganglia, LONG postganglionic fibers run all the way to target organs. The SNS has a high degree of neuronal DIVERGENCE: one preganglionic fiber can synapse with up to 20 postganglionic neurons. Thus, effects of the SNS tend to be WIDESPREAD.

In the PSNS, the preganglionic neurons arise from the brainstem and sacral region of the spinal cord. Preganglionic fibers exit the brainstem via several cranial nerves and exit the spinal cord via spinal nerves before forming the pelvic splanchnic nerves. Parasympathetic ganglia are located near or within target organs, so postganglionic fibers are relatively short. The degree of neuronal divergence in the PSNS is much lower than that of the SNS. Thus, the PSNS produces more SPECIFIC, LOCALIZED responses compared to the SNS.

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As undesirable as it might seem, PAIN is actually a very important defense mechanism. It WARNS the body about potential or actual injuries or diseases, so that protective actions can be taken. Basically, noxious signals send impulses to the spinal cord, which relays the information to the brain. The brain interprets the information as pain, localizes it, and sends back instructions for the body to react.

Pain sensation is mediated by pain receptors, or nociceptors, which are present in the skin, superficial tissues and virtually all organs, except for the brain. These receptors are essentially the nerve endings of so-called “first-order neurons” in the pain pathway. The axons of these neurons can be myelinated, A type, or, unmyelinated, C type. Myelinated A fibers conduct at FAST speeds and are responsible for the initial SHARP pain perceived at the time of injury. Unmyelinated C fibers conduct at SLOWER speeds and are responsible for a longer-lasting, dull, diffusing pain.

First-order neurons travel by way of spinal nerves to the spinal cord, where they synapse with second-order neurons in the dorsal horn. These second-order neurons cross over to the OTHER side of the cord, before ascending to the brain. This is how information of pain on the left side of the body is transmitted to the right side of the brain, and vice versa.

There are two major pathways that carry pain signals from the spinal cord to the brain:

– The spinothalamic tract: second-order neurons travel up within the spinothalamic tract to the thalamus where they synapse with third-order neurons; third-order neurons then project to their designated locations in the somatosensory cortex. This pathway is involved in LOCALIZATION of pain.

– The spinoreticular tract: second-order neurons ascend to the reticular formation of the brainstem, before running up to the thalamus, hypothalamus, and the cortex. This tract is responsible for the EMOTIONAL aspect of pain.

Pain signals from the face follow a DIFFERENT route to the thalamus. First-order neurons travel mainly via the trigeminal nerve to the brainstem, where they synapse with second-order neurons, which ascend to the thalamus.

Pain from the skin, muscles and joints is called SOMATIC pain, while pain from INTERNAL organs is known as VISCERAL pain. Visceral pain is often perceived at a DIFFERENT location in a phenomenon known as REFERRED pain. For example, pain from a heart attack may be felt in the left shoulder, arm or back, rather than in the chest, where the heart is located. This happens because of the CONVERGENCE of pain pathways at the spinal cord level. In this example, spinal segments T1 to T5 receive pain signals from the heart as well as the shoulders and arms, and the brain canNOT tell them apart. Because the superficial tissues have MORE pain receptors and are MORE often injured, it’s common for the brain to make an assumption that the pain comes from the shoulder or arm instead of the heart.

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Parkinson’s disease, or PD, is a neurodegenerative disorder in which DOPAMINE-producing neurons of a brain structure called the SUBSTANTIA NIGRA, are damaged and die over time, leading to a number of MOTOR problems and mental disabilities.

The substantia nigra is part of the basal ganglia, whose major function is to INHIBIT UNwanted motor activities. When a person intends to make a movement, this inhibition is removed by the action of dopamine. As dopaminergic neurons are progressively lost in PD patients, LOW levels of dopamine make it HARDER to INITIATE voluntary movements.

The events leading to neuronal cell death are poorly understood but the presence of so-called “Lewy bodies” in the neurons before they die may offer a clue and is currently the subject of intensive research.

Symptoms develop slowly over time; most prominent are MOTOR problems which include hand tremors, slow movements, limb rigidity and problems with gait and balance. These motor symptoms are collectively known as “PARKINSONISM”. However, parkinsonism may also be caused by a variety of other factors, which must be excluded before a person can be diagnosed with PD. Other motor-related problems may include slurred speech and reduced facial expressions. In later stages, non-motor symptoms such as mood and behavioral changes, cognitive impairment and sleep disturbances… may be observed.

The cause of Parkinson’s remains largely unknown but is likely to involve both genetic and environmental factors.

There is no cure for PD but current treatments are effective in managing motor symptoms:

First-line treatment involves medications which aim to INcrease dopamine levels in the brain. Major classes of medication include:

– Levodopa, a precursor of dopamine: levodopa can cross the blood brain barrier and is converted into dopamine inside the brain. Levodopa is the most effective of all medications but because it also produces dopamine elsewhere in the body, its side effects may become serious in the long-term. For this reason, levodopa is always administered together with some other drugs that inhibit its action OUTSIDE the brain.

– Dopamine agonists: substances that bind to dopamine receptors and mimic the action of dopamine.

– Another class of drugs includes INHIBITORS of enzymes that break down dopamine.

For people who do NOT respond to medications, surgery may be recommended. The most commonly performed procedure, deep brain stimulation, involves the implantation of a device called a neurostimulator, which sends electrical impulses to specific parts of the brain. By doing so, the device controls brain activities to relieve symptoms.