collection of neuron cell bodies located outside CNS

small molecule that incorporate a positively charge nitrogen atom: include AA, peptides and monoamines)/substances that inhibits or stimulate production of APs in post-synaptic membrane by binding to ligand gated ion channel; release from presynaptic membrane—diffuses across the synaptic cleft

  specialized structures /junction across which a nerve impulse ( or Action potential)passes from an axon terminal to a neuron, muscle cell, or gland cell

 occurs with conditions that impair the function of the blood-brain barrier: allowing transfer of water and protein from the vascular into the interstitial space

a.       Occurs in conditions: tumors, prolonged ischemia, hemorrhage, brain injury, and infectious processes (meningitis)

b.      Occurs primarily in white matter of the brain: white matter is more compliant than grey matter

c.       Can displace a cerebral hemisphere /responsible for several types of herniation

d.      Functional manifestations: focal neurologic deficits, disturbances in consciousness, and severe intracranial hypertension

     condition of increase in intracellular fluid as result from hypo-osmotic states such as water intoxication or severe ischemia that impair the function of the Na+/K+ membrane pump. Major changes in cerebral function such as stupor and coma. Edema associated w/ ischemia may produce cerebral infarction w/necrosis of brain tissue

 within the intracranial cavity

Determined by:

a.       Pressure-volume relationships among the brain tissue, cerebrospinal fluid (CSF), and blood in the intracranial cavity

b.      Monroe-Kellie hypothesis which relates to reciprocal changes among the intracranial volumes

c.       Compliance of the brain and its ability to buffer changes in intracranial volume

reciprocal relationship exists among the three intracranial volumes such that the ICP is maintained within normal limits.

a.       Volumes are incompressible, a change in one component must be balance by equal and opposite effect in one or both of the remaining components

b.      Fluid in the CSF compartment easily displaced: from ventricles and cerebral subarachnoid space to the spinal subarachnoid space/also undergo increased absorption or decrease production

c.       Blood in the cranial cavity contained in low pressure venous system/venous compression serves as a means of displacing blood volume.

displacement of brain tissue under the falx cerebri or through the tentorial notch or incisura of the tentorium cerebelli

a.       Occurs when an elevated ICP in one brain compartment cause displacement of the cerebral tissue toward an area of lower ICP

b.      Different types of herniation syndromes: divided into: supratentorial and infratentorial

enlargement of the CSF compartment; defined as an abnormal increase in CSF volume in any part or all of the ventricular system: Two causes (1) decrease absorption of CSF (2) overproduction of CSF; Two types: noncommunicating (or obstructive hydrocephalus occurs when obstruction in the ventricular system prevents the CSF from reaching the arachnoid villi) and communicating (caused by impaired reabsorption of CSF from the arachnoid villi into the venous system)

      recognized as a separate entity from panic disorder in DSMIII. The central characteristic of GAD is prolonged (6> month), excessive worry that is not easily controlled by the person.

a.       Characteristics include:

                                                              i.      Muscle tension

                                                            ii.      Autonomic hyperactivity

                                                          iii.      Vigilance and scanning (exaggerated startle response, inability to concentrate).

b.      Effective drug  treatment: benzodiazepines (eg chlordiazepoxide, diazepam); buspirone another effective drug (takes up to 2 weeks to show antianxiety effects and up to 6 weeks maximum benefits); SSRIs are also use (result in limbic, paralimbic and frontal hyperactivity normalization); other medications include antidepressant (tricyclic and atypical antidepressants) and b-adrenergic blockers

   anxiety disorder characterized by recurrent obsession 9repeated thoughts) and compulsions (repeated acts)/behavior (time consuming or distressing to individual). To be define as compulsive the behavior (activities such as  handwashing, ordering, or checking, or mental activities such as praying, counting , or repeating words) must be repeated excessively and the repetition must not be related to any environmental condition.

    (or social anxiety disorder), generalized or specific, intense, irrational, and persistent fear of being scrutinized or negatively evaluated by others. Diagnose criteria: development of symptoms of anxiety when the person is exposed to the feared social situation, recognition by the person of the social situation, and interference of the anxiety or avoidance behavior with the person’s normal routine. Fear not relate to any physiologic effects of a substance. Disorder must be present for at least 6 months.

(or non-normative cognitive decline that can be cause by any disorder that permanently damaged large association areas of cerebral hemispheres or subcortical areas sub-serving memory and learning.

a.       Essential feature of dementia: impairment of short- and long-term memory associated w/deficits in abstract thinking, impaired judgment, and other higher cortical functions, or personality change

b.      Disturbance sufficient to interfere w/work or social activities

c.       Common causes: Alzheimer disease, vascular dementia, frontotemporal dementia, Creutzfeldt-Jacob disease, Wernicke-Korsakoff syndrome, and Huntington chorea.

d.      Diagnisis: base on assessment of presenting problem, history (provided by informant), complete physical and neurologic examination, evaluation of cognitive, behavioral, and functional status; laboratory and imaging studies (CT or MRI); screening for depression, vitamin B12 deficiency and hypothyroidism.

e.       Depression is the most common treatable illness that may masquerade as dementia, and it must be excluded when a diagnosis of dementia is considered.

f.       Mnemonic DEMENTIA; Drugs (drugs with anticholinergic activity), Emotional (depression), metabolic (hypothyroidism), Eyes and ears (declining vision and hearing), Normal-pressure hydrocephalus, Tumor or other space-occupying lesions, Infection (HIV or syphilis), Anemia (B12 deficiency or folate deficiency)

Often referrred to as Lou Gehrig disease (cause- unknown), is a progressive disease that results in the death of nerve cell bodies in the brain and the spinal cord. When the motor neurons die, the ability of the brain to initiate and control muscle movement is lost. With voluntary muscle action progressively affected, patients in the later stages of the disease may becometotally paralyzed. As motor neurons degenerate, they can no longer send impulses to the muscle fibers that normally result in muscle movement. Early symtoms: increasing muscle weakness, especially involving the arms and legs, speech, swallowing or breathing. When muscles no longer receive the messages from the motor neurons that they require to function, the muscles being to atrophy (become smaller). Limbs begin to look "thinner" as muscle tissue atrophies. Later symptoms: paralysis, inability to swallow/eat, and inability to breathe deeply. Motor neuron damage can occur in any or all 3 areas: motor cortex, brain stem "bulbar", and spinal cord. Does not effect: sensation, coordination, ocular movement, cognition, bowel/bladder control. Respiratory failure/pneumonia common cause of death due to diaphragm paralysis. Primarily a disorder of middle to late adulthood (55-60 years of age) and men more than women; progressive disease that results in the death of nerve cell bodies in brain and spinal cord. When motor neurons die, the ability of the brain to initiate and control muscle movement is lost. Muscle action is progressively affected; in later stages muscle of palate, pharynx, tongue, neck and shoulders become involved, causing impairment of chewing, swallowing, and speech. Death follows w/involvement of cranial nerves and respiratory musculature; No cure, death 2-5 years from the onset of symptoms. Treatment requires management of medical problems, severe disability, and psychosocial problem are provided by multidisciplinary team/manage disorder symptoms (e.g. weakness and muscle spasms, dysphagia, communication difficulty, excessive watery saliva, and emotional liability), nutritional status, and respiratory muscle weakness (treatment allow patients to live longer). Theories of cause: chromosome mutation (increased free radicals), glutamate toxicity, autoimmune (but immunosuppressants don't work). Neuron cell bodies are damaged, sclerosed and die...leads to death, but usually over many years.

     is characterized by feelings of worthlessness and guilt, decreased concentration, alterations in sleep and appetite and possible suicidal ideation. Classified as unipolar (persistent unpleasant mood) and bipolar (alternating periods of depression and mania)

(idiopathic parkinsonism-dopamine depletion results from degeneration of the dopamine nigrostriatal system)- degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, and bradykinesia. Disorder characterized by progressive destruction of the nigrostriatal pathway, with subsequent reduction in striatal concentrations of dopamine. Usually begins after 50 years of age; clinical syndrome degenerative changes in basal ganglia function (refer as parkinsonism); Parkinsonism can develop postencephalitic syndrome which is a side effect of therapy w/antipsychotic drugs that block dopamine receptors, as a toxic reaction to a chemical agent, or as an outcome of severe carbon monoxide poisoning; Drug-induce parkinsonism follow administration of antipsychotic drugs in high doses (e.g. phenothiazines, butyrophenones)—these drugs block dopamine receptors and dopamine output by the cells of the substantia nigra; symptoms may be accompany w/cerebral vascular disease, brain tumors, repeated head trauma,  or degenerative neurologic disease that structurally damage the nigrostriatal pathway. Cardinal manifestations are tremor, rigidity, and bradykinesia or slowness of movement.

The basal ganglia provide background, involuntary movements, such as contracting muscles when you bend forward to keep you from toppling over. Many of the symptoms are caused by loss of this background balancing muscle contraction.

Basal ganglia Degeneration/Damage

• Substantia nigra (the basal ganglia affected)
• Loss of dopamine (80% loss before clinical manifestations)
• Unopposed Ach causes clinical manifestations (Dopamine is inhibitory and normally balances Ach in basal ganglia)

  Both ACETYLCHOLINE and DOPAMINE are released into SYNAPSES of the basal ganglia and normally balance each other. In Parkinson’s, there is a loss of DOPAMINE, leaving a relative excess of ACEYTLCHOLINE. (Thus, major medications to treat Parkinson’s include those that increase dopamine and combat acetylcholine.)

      presence of hypertension and bradycardia associated w/increased intracranial pressure. To perfuse the brain, the arterial blood pressure (represented as mean arterial pressure) must be greater than the intracranial pressure. Otherwise, the blood could not be pushed into the cranial vault and the brain would not be perfused with blood.  When the arterial pressure is LESS than the intracranial pressure, a reflex called the "CNS Ischemic Response" is initiated by the hypothalamus in the brain. The hypothalamus activates the sympathetic nervous system, causing peripheral vasoconstriction and an increase in cardiac output. These two effects serve to increase arterial blood pressure. When arterial blood pressure exceeds the intracranial pressure, blood flow to the brain is restored. The increased arterial blood pressure caused by the CNS ischemic response stimulates the baroreceptors in the carotid bodies, thus slowing the heart rate drastically — often to the point of a bradycardia.

    Demyelization (damage/loss of myelin) of neurons which slows or block nerve transmission along the neurons. Recall the myelin sheath is what allows nerves to transmit impulses at lightening speed. Myelin is damaged by inflammation. Characterized by inflammation and selective destruction of CNS myelin. Age onset 20-40 yrs of age; risk for developing MS is 15-fold higher when the disease is present in a 1^st degree relative and greater in monozygotic twins. Believe to be an immune-mediated disorder that occurs in genetically susceptible people. Lesions of MS consist of hard, sharp-edged, demyelinated or sclerotic patches that are macroscopically visible throughout the white matter of the CNS. Clinical manifestations: demyelination of nerve fibers in the white matter of the brain, spinal cord, and optic nerve. CNS myelin is formed by olingodendrocytes (function is equivalent to Schwann cells in the PNS), chiefly those lying among the nerve fibers in the white matter. Some myelin is replaced with sclerotic plaque (like scar tissue), may heal during remissions (then nerve can function again). Autoimmune etiology. CD4 and CD8 T-cells injure oligdendrocyte (cells that produce myelin). Strong link to HLA (human leukocyte antigen). Viral/bacterial infection may trigger MS in those predisposed. Exacerbations (flare up) and remissions (periods of no S/S) is the typical patter. Early S/S: parathesia arm/leg (numbness/tingling), weak, dizzy, fatigue, diploplia, blurred vision (often first sign). Later more severe symptoms: muscle spasms, paralysis, bowel/bladder and sexual problems, slurred speech, blindness, confusion/forgetfulness. Upper motor axons (in CNS- brain or cord) are sclerosed but can heal during remissions...ultimately cannot heal...leads to death in months to a few years.

   Chronic autoimmune neuromuscular disease characterized by varying degrees of weakness of the skeletal (voluntary) muscles of the body.  Literally means "grave muscle weakness". With current therapies, however, most cases are not as "grave" as the name implies. The majority of individuals, life expectancy is not lessened by the disorder. Hallmark of myasthenia gravis is muscle weakness that increases during periods of activity and improves after periods of rest. Certain muscles such as those that control eye and eyelid movement, facial expression, chewing, talking, and swallowing are often, but not always, involved in the disorder. The muscles that control breathing and neck and limb movements may also be affected. Myasthenia gravis is caused by a defect in the transmission of nerve impulses to muscles in which antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction preventing the muscle contraction from occurring. Antibodies are produced by the body's own immune system, thus myasthenia gravis is an autoimmune disease because the immune system - which normally protects the body from foreign organisms - mistakenly attacks itself. SIGNS & SYMPTOMS / PROGNOSIS

a.       Muscle weakness & fatigue with sustained effort or activity (improves after rest)

b.      Eye & face muscles EARLY symptoms (ptosis, diplopia, chewing, swallowing & speech problems)

c.       Proximal limb weakness (trouble lifting objects or climbing stairs)

d.      Symptoms LEAST in MORNING, WORSEN as day progresses

e.       With treatment, expect to lead normal life

caused by a defect in the transmission of nerve impulses to muscles. It occurs when normal communication between the nerve and muscle is interrupted at the neuromuscular junction (synapse) - the place where nerve cells connect with the muscles they control. Normally when impulses travel down the nerve, the nerve endings release a neurotransmitter called acetylcholine. Acetylcholine travels through the neuromuscular synapse and binds to acetylcholine receptors which are activated and generate a muscle contraction.

antibodies block, alter, or destroy the receptors for acetylcholine at the neuromuscular junction, which prevents the muscle contraction from occurring. Antibodies are produced by the body's own immune system, thus myasthenia gravis is an autoimmune disease because the immune system - which normally protects the body from foreign organisms - mistakenly attacks itself.

 (stroke) three types (1) ischemic- brain injury die to blockage of blood flow to areas of the brain (2) hemorrhagic- brain injury due to bleeding into brain tissue (3) global hypoperfusion- lack of perfusion to the entire brain, often related to pathology outside of the brain (eg shock)

Central Nervous System

composed of brain and spinal cord

3 regions of the brain: the hindbrain, the midbrain, and the forebrain

Hindbrain

 art of the brain stem (along with midbrain), includes the cerebellum, medulla oblongata, and pons; have organization of spinal cord segments; can be called rhombencephalon

                                                        Cerebellum

develops in fifth neural tube segment; functions to relay signals from the cortex to assist in the control of movement and is also involved with the control of sleep and arousal. It connects the midbrain to the medulla; abducens and trigeminal nerves emerge through pons

Medulla oblongata

involved with the control of unconscious, essential functions such as breathing, blood circulation and muscle tone. It connects the pons to the spinal cord; Hypoglossal, vagus, glossopharyngeal, spinal accessory, vestibulocochlear, facial nerves emerge from or around medula.

Stroke (CVA) in cerebellum

can occur in cerebellum, medulla, or pons

Brain Stem

 dorsal and ventral side- the dorsal side contains colliculi (small protuberances that are involved in vision and hearing) and the ventral side contains the cerebral peduncles which divide the brain into two parts. This is composed of a strip of grey matter (containing neurons which help transmit motor signals) called the substantia nigra; stroke can occur here

Disorder that affects substantia nigra

 Parkinson’s disease

Forebrain

 contains the largest part of the brain including the cerebrum, the thalamus, the hypothalamus, and the limbic system.

Diencephalon

 Composed of thalamus and hypothalamus, optic nerve and retina are outgrowths of the diencephalon

 group of myelinated axons located on either side of the internal capsule, just lateral to the thalamus; composed of comma-shaped caudate nucleus, shild-shaped putamen, and the globus pallidus; the striatum refers to the caudate plus the putamen, lentiform nucleus refers to the globus pallidus and putamen; supplies axial and proximal unlearned and learned posture and movements; provide arm swinging during walking or running, follow through movements, nuclei on rights side provide movements to the left side of the body; (frequent or continuous movements that occur with Parkinson’s disease, Huntington chorea, and some forms of cerebral palsy result from basal ganglia dysfunction)

Cerebrum

Cerebral cortex  

 Grey matter covering cerebrum; gyrus (ridge between two groups, the mountain), sulcus (groove or valley on each side of the gyrus), fissure (deeper grooves and the sulcus)

Temporal lobe

 memory, hearing, understanding language, and processing information

Parietal lobe

Frontal lobe

extends from the frontal pole to the central sulcus and is separated from the temporal lobe by the lateral sulcusthe emotional control, self awareness, motivation, Judgment, Problem solving, talking, movement, initiation

Occipital lobe – vision

Thalamus

 relay sensory information to the cerebral cortex and the hypothalamus regulates visceral functions, such as temperature, reproductive functions, eating, sleeping and the display of emotion.

Cerebral cortex disorders

Disorders that affect cerebrum

 Alzheimer's disease, depression, mania

Disorders that affect parietal

Disorders that affect the Limbic system

Disorders that affect hippocampus

Spinal Cord

– extends from the base of the brain, at the foramen magnum, to the level of the 1^stor 2^nd lumbar vertebra; it is surrounded (and protected) by the vertebral column and is composed of gray and white matter. There is transmission, both ascending and descending, through the afferent and efferent impulses

Afferent impulses

– or sensory neurons carry information to the CNS

Efferent impulses

Spinal nerves

- the peripheral nerves that carry information to and from the spinal cord. Usually there are 32 or more pairs which include 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 2 or more coccygeal

– protective membranes that cover the brain and spinal cord: dura mater (2 layers), arachnoid, pia mater

Spinal cord

– upper two thirds of spinal column, protected by vertebral column, extends from foramen magnum at the base of the skull to a cone-shapedtermination, the conus medullaris.

- composed of strong connective tissue and is the outermost layer of the meninges

Arachnoid  

- the second layer of the meninges and is nonvascular and contains the CSF (cerebrospinal fluid) in the subarachnoid space; this circulates through the entire CNS

Pia mater

- the innermost layer and contains both the surface blood vessels and those that penetrate the brain and spinal cord

Subdural space

- another area where blood collections can occur due to the venous system that runs through this layer and empties into the internal jugular system and returns to the heart

Neuron  

- The functional cell of the nervous system, composed of the axon, dendrite, and cell body

Glial cells

– in PNS

- produced by some of cells in both the CNS (glial) and PNS (schwann); this is composed of lipid content and gives the name “white matter” to fibers in the spinal cord and brain. It is protective and also helps with increasing the speed of impulse conduction

- chemical messengers that are manufactured, stored, and released at the synapses and bind to the receptors on a neuron (usually the one that follows the

one that released it) - with this binding, depending on the type of receptor, the neuron is either stimulated or inhibited to pass along a signal. If a neuron is stimulated to pass along a signal, it does this through ion channels that help change the “excitability” of the neuron. Signals can be passed in this way from neuron to neuron through chemical synapses

Synapses

- the junction across which a nerve impulse passes from an axon terminal to a neuron

Common neurotransmitters that are involved in diseases with the neurological system

- dopamine, acetylcholine, and serotonin; Many of the medications that are prescribed for the neurological system either enhance, replace, or inhibit the effects of these

Dopamine

- Involved in a wide variety of behaviors and emotions, including pleasure. Implicated in schizophrenia and Parkinson’s disease.

- Distributed widely throughout the central nervous system, where it is involved in arousal, attention, memory, motivation, and movement. Involved in muscle action through presence at neuromuscular junctions (specialized type of synapse where neu- rons connect to muscle cells). Degeneration of neurons that produce ACh have been linked to Alzheimer’s disease. Too much can lead to spasms and tremors; too little, to paralysis or torpor; for preganglionic neurons for both ANS divisions,and the postganglionic neurons of the parasympathetic nervous system

- an important part of the nervous system that involves neurotransmitters. It is an efferent system that is involuntary and is responsible for maintaining the homeostatic functions of the body. This involves automatic running of our vital functions such as blood flow, respirations, body temperature, digestion, metabolism and elimination. It is also involved when there are threats to a person in what is called the“fight and flight” response. There are two divisions in this system: the sympathetic and parasympathetic divisions.

– (internal and peripheral actions), Maintains vital functions, Responds when there is a critical threat to the integrity— the“flight or fight” response, Motor/sensory. located in the intermediolateral horn of the spinal cord between T1 and L2 or L3. The sympathetic ganglia are adjacent to the spine and consist of the vertebral (sympathetic chain) and prevertebral ganglia, including the superior cervical, celiac, superior mesenteric, inferior mesenteric, and aorticorenal ganglia. Long fibers run from these ganglia to effector organs, including the smooth muscle of blood vessels, viscera, lungs, scalp (piloerector muscles), and pupils; the heart; and glands (sweat, salivary, and digestive).

                                                     Parasympathetic

- consist of 2 sets of nerve bodies: one set (called preganglionic) in the CNS, with connections to another set in ganglia outside the CNS. Efferent fibers from the ganglia (postganglionic fibers) lead to effector organs

                                     Norepinephrine and epinephrine

                    Symptoms suggesting autonomic insufficiency include

- Orthostatic hypotension, Heat intolerance, Loss of bladder and bowel control, Erectile dysfunction (an early symptom), Other possible symptoms include dry eyes and dry mouth, but they are less specific.

Lab testing for someone showing symptoms and signs suggesting autonomic insufficiency - sudomotor, cardiovagal, and adrenergic testing is usually done to help determine severity and distribution of the insufficiency.

Sudomotor

- Quantitative sudomotor axon-reflex test: This test evaluates integrity of postganglionic neurons using iontophoresis; electrodes filled with acetylcholine are placed on the legs and wrist to stimulate sweat glands, and the volume of sweat is then measured. The test can detect decreased or absent sweat production.Thermoregulatory sweat test: This test evaluates both preganglionic and postganglionic pathways. After a dye is applied to the skin, patients enter a closed compartment that is heated to cause maximal sweating. Sweating causes the dye to change color, so that areas of anhidrosis and hypohidrosis are apparent and can be calculated as a percentage of BSA.

                                                    Cardiovagal

                                                        Adrenergic

                                               Plasma norepinepherine

–olfactory; sense of smell

Cranial nerve II

– oculomotor; papillary reflex, extrinsic muscle movement of eye; test by using penlight to assess pupillary direct and consensual responses to light, test accommodation

                                                   Cranial nerve IV

                                                 Cranial nerve V

Testing III, IV, VI

– asses extraocular movement by during the “H”

                                                           Cranial nerve VI

                                                      Cranial nerve VII

                                                       Cranial nerve IX

                                                     Cranial nerve X

                                                          Test IX & X

                                                        Cranial nerve XI

                                                      Cranial nerve XII

–hypoglossal; movement of tongue for swallowing, movement of food during chewing and speech; test: instruct patient to stick tongue out & move side to side, ask them to provide resistance against your finger with tongue inside cheek on both sides

-Chronic disorder of the CNS where myelin and nerve axons in the brain and spinal cord are destroyed

Most prominent in women and European-American

-Exacerbation of the illness can be precipitated by stress, pregnancy illness, fever, fatigue.

Destruction of myelin and nerve axons causes a temporary, repetitive, or sustained interruption in the conduction of nerve impulses which causes the symptoms of MS

-Plaque formation occurs throughout the white matter of the CNS which also affects the nerve impulses; affects the optic nerves, cervical spinal cord, thoracic and lumbar spine

-Inflammation occurs around the plaques as well as normal tissue; astrocytes (gliosis) appear in the lesions and scar tissue forms, replacing the axon and leading to permanent disability: the term “gliosis” leads to the term sclerosis which means scaring

-the immune response: Helper T-cells are elevated in CSF at the onset; T-suppressor cells are decreased in serum before and during an exacerbation of illness;

Motor, sensory, cerebellar, and emotional problems

-weakness or paralysis of the limbs, trunk, or head; Diplopia; scanning speech; spasticity of muscles that are chronically affected

-Sensory abnormalities include numbness and tingling and othe parathesias, patchy blindness (scotomas), blurred vision, vertigo, tinnitus, decrease hearing, and chronic neuropathic pain

-Cerebellar signs include nystagmus, ataxia, dysarthria, and dysphagia

-Sclerotic plague may be in areas that control elimination/bowel, bladder and sexual dysfunction

4 forms based on the rate of progression:

-benign (nervous system dysfunction in different episodes; full recovery follows)

-relapsing-remitting (most common: neurological exacerbations occur/improvement seen either complete or partial recorvery)

-primary progressive (sudden loss of neurological function/may resolve; leave severe functional impairments—worsen over time/no remission follows),

-secondary progressive (starts similar to relapsing-remitting; changes to a primary progressive form; no remission follows)

History and physical examination (analysis of complains, neurovascular assessment, movement, mental assessment, and eye exam)

CSF analysis (clonal IgG bands present)

Muscle testing

CT scan

MRI, MRS

Lou Gehrin disease

-Degenerative disease of the upper and lower motor neurons of the cerebral cortex, brain stem, and spinal cord that results in paralysis (except for cranial nerves III, IV, & VI)

-Causes are unknown, viral infections, metabolic disorders, and trauma; familial patterns and autoimmune responses

-Primarily a disorder of middle to late adulthood (55-60 years)

-Progressive course w/ a mean survival period of 2-5 years

-No cure

Motor neurons in the cortex, brain, stem, and spinal cord are lost; non-inflammatory; axon degeneration causes demyelination

Effect on UMN function leads to spastic, weak muscle, and increased deep-tendon reflexes

Effect on LMN function causes muscle atrophy and flaccid paralysis

Advance stages muscles of the palate, pharynx, tongue, neck, and shoulders become involved, causing impairment of chewing swallowing, and speech.

Dysphagia w/recurrent aspiration and weakness of respiratory muscles produces the most significant acute complications of the disease.

Death results from involvement of cranial nerves and respiratory musculature.

- Muscle cramps involve the distal legs often an early symptom

-Symptoms referable to UMN or LMN

-Manifestation of UMN lesions include weakness spasticity or stiffness, and impaired fine motor control

Dysphagia (difficulting swallowing), dysarthri (impaired articulation of speech), and dysphonia (difficulty making the sound of speech) may result from brain stem LMN involvement or dysfunction of UMNs descending to the brainstem

-Manifestations of LMN destruction include fasciculations, weakness, muscle atrophy, and hyporeflexia.

Acute (sudden onset), rapidly progressing limb weakness and loss of tendon reflexes; most common cause of acute, flaccid paralysis;

inflammation of peripheral motor and sensory nerves characterized by : variable motor weakness and paralysis; paralysis that ascends symmetrically from lower extremities;

Causes are unknown; autoimmune attack, common after viral infections, immunizations, febrile illness, injury or surgery

Medical emergency (rapid development of ventilator failure and autonomic disturbances that threaten circulatory function

2/3 cases occur after a viral infection

Temporary demyelination of peripheral nerves that results in the skeletal muscle weakness and paralysis

Several subtypes: pure motor axonal degeneration, axonal degeneration of both motor and sensory nerves, and variant characterized by ophthalmoplegia, ataxia, and areflexia.

80-90% of people spontaneous recover within 6-12 months.

Paralysis of respiratory muscles; required ventilator assistance.

Autonomic disturbances that threaten circulatory function

Medical history

spinal tap (lumbar puncture) and nerve function tests (Electromyography, Nerve conduction studies)

Disorder of transmission at the neuromuscular junction that affects communication b/w motor neuron & innervated muscle cell.

Autoimmune disease

o Antibodies formed against Ach receptors

o Thymus implicated - may give incorrect instructions to developing immune cells,

 Result is a WEAK muscle response to Ach release

 Increasing Ach level improves symptoms (more Ach to activate more receptors, some of which are normal)

Autoimmune response/unclear thought to be cause by sensitized helper T cells and an antibody-direct attack on the acetylcholine receptors in the neuromuscular junction

-75% w/MG also have thymic abnormalities (e.g. thymoma—thymic tumor), or thymic hyperplasia (e.g. ­ thymus weight from an ­ # of thymus cells) and Neonatal MG occur 10% newborns to mothers w/disease (spontaneous resolution within few month of birth)

Eye & face (Ptosis, Diplopia, chewing, swallowing & speech problems)

-Muscle weakness & fatigue w/sustained effort or activity (improve after rest)

Myasthenic crisis: sudden exacerbation of symptoms and weakness; occurs when muscle weakness becomes severe enough to compromise ventilation to the extent the ventilator support and airway protection are needed; this occur during period of stress such as infection, emotional upset, pregnancy, alcohol ingestion, cold exposure or surgery; or result from inadequate or excessive doses of the anticholinesterase drugs use to treat disease

Less evident in the morning but grow worse w/effort and as day progresses. With treatment expect to lead normal life

Ocular muscle weakness to generalized weakness, including respiratory muscle weakness, chewing and swallowing.

Weakness of limb movement/pronounce in proximal parts than distal parts of extremities

-muscles of lower face are affected causing speech impairment

History and physical

-anticholinesterase test

-Electrophysiologic studies

-Single-fiber electromyography

-Immunoassay test

Progressive gradual neurological degenerative disorder of basal ganglia function that results in variable combination of tremor, rigidity and bradykinesia.

Causes are:

-Idiopathic (unknown causes)

-Antipsychotic medications (block dopamine)

-After episodes of—encephalitis, CO poisoning, brain injury/trauma

-Genetic mutation/if early onset (< 45 yrs of age)

Affects brain centers that control and regulate movement

-neurons in substantia nigra and corpus striatum in midbrain degenerate and become deficient in production and storage of neurotransmitter dopamine

-When dopamine levels that inhibit motor activity deplete, acetylcholine is not inhibited allowing increased excitation that is the basis of symptoms of Parkinson’s disease

deficits in executive functioning may be among earliest signs of cognitive decline, as evidenced by difficulty in planning, starting and carrying out tasks

- only mild tremor, a slight limp, or decrease arm swing may be evident

-slight change in speech patterns

Weight loss, constipation, dysphagia, depression and dementia

-Tremors: “pill rolling” nonintentional tremor of thumb; begin in one hand and spread to arm, then othe arm, and later head; lessens w/purposeful movement

-Bradykinesia and loss of autonomic movement characterized w/masklike face w/staring gaze; soft, monotone voice; drooping of saliva; impaired balance and loss of righting reflex (correcting posture when changing positions); stooped posture; difficulty initiating movement; unsteady shuffling propulsive gait

-Rigidity: cogwheel (manual manipulation of the body parts); increase resistance to passive ROM w/jerky catches when joint is move/Lead pipe: cataleptic condition during which limbs remain in any position in which place; smooth, stiff movement

-Autonomic dysfunction: insomnia, oily skin, sweating, heat intolerance, orthostatic hypotension

    head injury in which the skull is fractured, develops between the inner table of the bones of the skull and the dura. It usually results from a tear in an artery (middle meningeal), bleeding is arterial which causes rapid expansion. It is more common in younger persons because the dura is less firm. Persons present a history of head injury and a brief period of unconsciousness followed by a lucid period which conscious is regained, followed by a rapid progression to unconsciousness. 

Symptoms – ipislateral pupil dilation and contralateral hemiparesis from uncal herniation.  Increased ICP, tentorial herniation and death occur if the hematoma is not removed

·         develops in the area between the dura and the arachnoid (bleeding can occur there and or into the CSF-filled subarachnoid space)from a tear in the small bridging veins that connect veins on the surface of the cortex to dural sinuses. Venous source of bleeding I a subdural hematoma develops more slowly than the arterial epidural hematoma.

1.       Acute subdural hematoma – progress rapidly, high mortality rate because of the severe secondary injuries related to edema and increased ICP. High mortality rate is due to uncontrolled ICP rate, loss of consciousness, decerebrate posturing and delay in surgical removal. Symptoms develop within 24 hours

2.       Subacute subdural hematoma – period of improvement in the level of consciousness and neurologic symptoms only following deterioration if the hematoma is not removed. Symptoms develop 2 to 10 days after injury.

3.       Chronic subdural hematoma – More common in older persons because brain atrophy shrinks away from the dura and stretch fragile bridging veins. The veins rupture, causing slow seepage of blood into the subdural space. Fibroblastic activity causes the hematoma to become encapsulated. The sanguineous fluid in this area has high osmotic pressure and draws in fluid from the surrounding subarachnoid space; the mass expands, exerting pressure on the cranial contents. Sometimes the clinical picture is less defined, with prominent symptoms being a decreasing level of consciousness indicated by drowsiness, confusion, headache and apathy.

·         single or multiple, occur in any lobe but are common in frontal or temporal lobes, related to the bony prominences on the inner skull surface. Occur in older persons and alcoholics whose cerebral vessels are more friable.

§  Symptoms – depending on size.

§  Large and encroaching on vital structures –increased ICP

§  Temporal lobe- dangerous, potential for lateral herniation.

§  Surgery may not be needed in someone who is neurologically stable despite neurologic deficits; the hematoma may resolve like a contusion

·         caused by cerebrovascular obstruction by thrombosis or emboli. A common classification system indentifies the five main mechanisms of stroke as stroke subtypes and their frequency

1.       20% large artery atherosclerotic disease (both thrombosis and arterial emboli)

2.       25% small vessel or penetrating artery disease (lacunar stroke)

3.       20% cardiogenic embolism

4.       30% cryptogenic stroke (undetermined cause)

5.       5% other, unusual causes (migraine, vessel dissection, coagulopathy)

§  In evolution of a stroke, a central core of dead or dying cells. Surrounded by an ischemic band or area of minimally perfused cells called the penumbra. Brain cells of the penumbra receive marginal blood flow and their metabolic activities are impaired; the area undergoes “electrical failure,” the structural integrity of the brain cells is maintained. Survival of these cells depend on the return of adequate circulation, the volume of toxic products released by neighboring dying cells, the degree  of the cerebral edema, and alterations in local blood flow.

§  common cause of ischemic strokes, usually occurring in atherosclerotic blood vessels, which are found most commonly at arterial bifurcations. Common sites of plaque formation include larger vessels of the brain, notably the origins of the internal carotid and vertebral arteries, and junctions of the basilar and vertebral arteries. Cerebral infraction can result from an acute local thrombosis and occlusion at the site of chronic atherosclerosis, with or without embolization of the plaque material distally, or from critical perfusion failure distal to a stenosis (watershed).

-        These infarcts often affect the cortex – causing aphasia or neglect, visual field defects, or transient monocular blindness (amaurosis fugax).

-        Occurs commonly in older persons and frequently accompanied by evidence of atherosclerotic heart or peripheral arterial disease. It is not associated with activity and may occur in a person at rest.

§  small infarcts located in the deeper, noncortical parts of the brain or in the brain stem.

-        Found in the territory of single deep penetrating arteries supplying the internal capsule, basal ganglia, or brain stem resulting from occlusion of the smaller penetrating branches of large cerebral arteries, commonly the middle cerebral and posterior cerebral arteries.

-        During healing, lacunar infarcts leave behind small cavities, or lacunae. These result from arteriolar lipohyalinosis or microatheroma, commonly in the settings of chronic hypertension or diabetes. They do not cause cortical deficits like aphasia or apraxia due to their size and location but do produce classic recognizable “lacunar syndromes” such as pure sensory hemiplegia and dysarthria with the clumsy hand syndrome. Six basic causes are

1.       Embolism

2.       Hypertension

3.       Small vessel occlusive disease

4.       Hematologic abnormalities

5.       Small intracerebral hemorrhages

6.       Vasospasm

§  moving blood clot that travels from its origin to the brain, usually affecting the larger proximal cerebral vessels, often lodging at bifurcations having a sudden onset with immediate maximum deficit. The middle cerebral artery is the most frequent site of embolic strokes. Most cerebral emboli originate from a thrombus in the left heart; they also originate in an atherosclerotic plaque in the carotid arteries. 

-        Cardiac conditions predispose to formation of emboli that produce embolic stroke such as

§  Rheumatic heart disease

§  Atrial fibrillation

§  Recent myocardial infarction

§  Ventricular aneurysm

§  Mobile aortic arch atheroma

§  Bacterial meningitis

·         fatal, occurs suddenly, spontaneous stroke that results in an intracerebral hemorrhage with rupture of the blood vessel, hemorrhage into the brain tissue  resulting in a focal hematoma and sometimes intraventricular hemorrhage, edema, compression of the brain contents, or spasm of the adjacent blood vessels.

-        Common factors – advancing age and hypertension.

-        Other causes – aneurysm, trauma, erosion of the vessels by tumors, arteriovenous malformations, blood coagulation disorders, vasculitis, and drugs.

-        Vomiting commonly occurs at onset and a headache often occurs.

-        Focal symptoms depend on which vessel is involved.

-        Hemorrhage into the basal ganglia results in contralateral hemoplegia, with initial flaccidity progressing to spasticity.

-        The hemorrhage and resultant edema exert great pressure on the brain substance, and the clinical course progresses rapidly to coma and frequently to death.

·         Major risk factors for stroke are age, sex, family history, hypertension, smoking, diabetes, asymptomatic carotid stenosis, sickle cell disease, hyperlipidemia, atrial fibrillation.

·         African Americans have almost twice the risk of strokes as whites.

·         Blood pressure is a powerful dominant of stroke risk. Persons with lower 120/80 mm Hg have half the lifetime risk of strokes compared to hypertension.

·         Heart disease: atrial fibrillation and other conditions that predispose to clot formation on the wall of the hearts or the valve leaflets or paradoxical embolism through right-to-left shunting, predisposes to cardioembolic stroke.

·         Polycythemia, sickle cell disease (during sickle cell crisis), and blood disorders predispose to clot formation in the cerebral vessels.

·         Obesity, physical inactivity, alcohol and drug abuse, hypercoagubality disorders, hormone replacement therapy and oral contraceptive use are less well-documented risk factors.

·         Estrogen plus progestin increase stroke in postmenopausal, generally in healthy women and provide no protection for women with established heart disease.

·         Alcohol: induction of cardiac arrhythmias and defects in ventricular wall motion that lead to cerebral embolism, induction of hypertension, enhancement of blood coagulation disorders, and reduction of cerebral flow.

·         Cocaine use causes both kind of strokes by inducing vasospasm, enhanced platelet activity, and increased blood pressure, heart rate, body temperature, and metabolic rate. Cocaine stroke victims range in age from newborn to elderly.

·         Primary (direct) brain injuries are caused by impact, include diffuse axonal injury and the focal lesions of laceteration, contusion, and hemorrhage.

·         Secondary brain injuries results from the subsequent brain swelling, infection, or cerebral hypoxia. They are often diffuse or multifocal, including concussion, infection, and hypoxic injury.

§  Ischemia is the major cause of secondary brain injury.

§  It can result from the hypoxia and hypotension that occur during the resuscitation process or from the impairment of regulatory mechanisms by which cerebrovascular responses maintain an adequate blood flow and oxygen supply.

§  Significance of secondary injuries depends on the extent of damage caused by the primary injury.

·         This occurs when the mechanical forces inducing head injury cause bouncing of the brain in the closed confines of the rigid skull.

·         Coup injury: direct contusion of the brain at the site of external force

·         Contrecoup injury: rebound injury on the opposite side of the brain

·         Contusions and hematomas result when the brain strikes the rough surface of the cranial vault, brain tissue, blood vessels, nerve tracts, and other structures are bruised and torn.

·         ICP can be caused by a volume change in any of the three intracranial components: Cranial cavity contains blood (10%), brain tissue (80%), and CSF (10%).

·         Increase in tissue volume can result from a brain tumor, brain edema, or bleeding into brain tissue

·         Increase in blood volume develops when there is  vasodilation of cerebral vessels or obstruction of venous outflow

·         Excess production, decreased absorption, or obstructed circulation of CSF affords the potential for an increase in the CSF component.

·         Tissue volume is relatively restricted in its ability to undergo change; CSF and blood volume are best able to compensate for changes in ICP.

·         Initial increases in ICP are buffered by a translocation of CSF to the spinal subarachnoid space and increased reabsorption of CSF.

·         Hypertension, bradycardia, widened pulse pressure are the important but late indicators of increased ICP

·         Triggered by ischemia of the vasomotor center of the brain stem; neurons produce a mark increase in MABP in an attempt to increase CPP sometimes to levels as high as 270 mm Hg, accompanied by a widening of the pulse pressure and reflex slowing of the heart rate.

Brain herniation represents a displacement of brain tissue under the falx cerebri or through the tentorial notch or incisura of the tentorium cerebelli.

Supratentorial, Infratentorial

§  Cingulate – less serious threat in terms of clinical outcomes and it involves displacement of the cingulated gyrus and hemisphere beneath the sharp edges of the falx cerebri to the opposite side of the brain. Displacement of the falx can compress the local brain tissue and blood supply from the anterior cerebral artery, causing ischemia and edema, which further increases ICP levels. Leg weakness is an early sign of cingulate herniation.  

§  Central transtentorial – result in two distinct syndromes: an uncal syndrome and a central syndrome and it involves the downward displacement of the cerebral hemispheres, basal ganglia, diencephalon, and midbrain through the tentorial incisura.

-        The diencephalon may be compressed tightly against the midbrain with force that edema and hemorrhage result.

-        The first sign of central herniation is clouding of consciousness which is caused by pressure on the reticular activating system in the upper midbrain, which is responsible for wakefulness.

-        Early diencephalic stage: clouding of consciousness, bilaterally small pupils with a full range of constriction and motor responses to pain that are purposeful or semi purposeful and often asymmetric occurs.

-        Late diencephalic stage: Painful stimulation results in decorticate posturing, which may be asymmetric and there is waxing and waning of respirations with periods of apnea (Cheyne-Stokes respirations). With midbrain involvement, the pupils are fixed and midsized, reflex adduction of the eyes is impaired; pain elicits decerebrate posturing; respirations change from Cheyne-Stokes to neurogenic hyperventilation (>40 breaths per minutes because of uninhibited stimulation of the Inspiratory and expiratory centers).

-        With lower pons and upper medulla involvement, pupils are fixed and midpoint with loss of reflex abduction and adduction of the eyes and absence of motor responses or only leg flexion on painful stimuli.

-        When the herniation is beyond the diencephalon and into the midbrain and brain stem, the process is irreversible and the prognosis poor.

§  Uncal transtentorial - occurs when lateral mass pushes the brain tissue centrally and forces the medial aspect of the temporal love, which contains the uncus and hippocampal gyrus, under the edge of the tentorial incisura, into the posterior fossa. The diencephalon and midbrain are compressed and displaced laterally to the opposite side of the tentorium. Cranial nerve III (oculomotor nerve) and the posterior cerebral artery frequently are caught between the uncus and the tentorium.

-        Oculomotor nerves control pupillary constriction. Entrapment of this nerve results in ipsilateral papillary dilation which is an early sign of uncal herniation.

-        As uncal herniation progresses, changes in motor strength and coordination of voluntary movements occurs because of compression of the descending motor pathways. It can occur on the same side of the brain damage because of the compression of the contralateral cerebral peduncles. Bilateral babinski responses and respiratory changes (Cheyne-Stokes respirations, ataxic patters) occurs. Decorticate and decerebrate posturing may develop, followed by dilated, fixed pupils, flaccidity and respiratory arrest.

·       results from increased pressure in the Infratentorial compartments and can progress rapidly and cause death because it is likely to involve the lower brain stem centers that control vital cardiopulmonary functions. Herniation may occur superiorly (upward) through the tentorial incisura or inferiorly (downward) through the foramen magnum.

-        Upward- blockage of the aqueduct of Sylvius and lead to hydrocephalus and coma.

-        Downward – interfere with medulla functioning and cause cardiac or respiratory arrest.

-        Preexisting ICP elevations, herniation may occur when the pressure is released from below, such as a lumbar puncture.

-        If the CSF pathway is blocked and fluid cannot leave the ventricles, the volume expands and fluid is displaced downward through the tentorial notch. The expanding volume causes all function at a given to cease as destruction professes in a rostral-to-caudal direction.

-        The result is brain stem ischemia and hemorrhage extending from the diencephalon to the pons.

·         Disorder of transmission at the neuromuscular junction that affects communication between the motor neuron and the innervated muscle cell. 20-30 years of age is the peak, three times more common in women than men.

·         Lambert-Eaton myasthenic syndrome is a special type of myasthenic syndrome that develops in association with neoplasms, small cell carcinoma in the lungs

·         Autoimmune disease caused by an antibody-mediated loss of acetylcholine receptors in the neuromuscular junction.

·         Symptoms – muscle weakness, fatigability commonly affecting the eye and periorbital muscles with ptosis due to eyelid weakness or diplopia due to weakness of the extraocular muscles. Ocular muscle weakness to generalized weakness, respiratory muscle weakness. Difficulty in chewing and swallowing and weakness in limbs. Muscles of lower face are affected causing speech impairment. Symptoms are least evident in the morning but are worse as the day progresses.

·         Myasthenic crisis occurs when muscle weakness becomes severe enough to compromise ventilation to the extent that ventilatory support and airway protection are needed. Occurs during stress, infection, emotional upset, pregnancy, alcohol cold, inadequate or excessive doses of the anticholinesterase drugs.

·         Demeylinating disorder by inflammation and selective destruction of CNS myelin (nerve fibers in the white matter of the brain, spinal cord, and optic nerve).  People with the human leukocyte antigen HA-DR2 haplotype are particularly susceptible.

·         Immune mediated disorder that occurs genetically, immune response to a protein in the CNS.

·         Lesions of MS are hard, sharp-edged, demyelinated or sclerotic patches that are macroscopically visible throughout the white matter of the CNS. The lesions represent the end result of acute myelin breakdown called plaques.

·         Lesions have a predilection for the optic nerves, periventricular white matter, brain stem, cerebellum, and spinal cord white matter.

·         Lesions contain small amounts of myelin basic proteins and increased amounts of proteolytic enzymes, macrophages, lymphocytes, and plasma cells. Oligodendrocytes are decreased and may be absent.

·         Disease of motor function, mean of survival 2 to 5 years from the onset of symptoms.

·         Affects motor neurons in the

1. Anterior horn cells of the spinal cord  - death of LMNs leads to denervation, with subsequent shrinkage of musculature and muscle fiber atrophy.

2. Moto nuclei of the brain stem, the hypoglossal nuclei

3. UMNs of the cerebral cortex.

·         The gene for a subset has been mapped to superoxide dismutase 1 on chromosome 21.

·         ALS due to exotoxic injury through activation of glutamate-gated ion channels, which are distinguished by their sensitivity to N-methyl-D-aspartic acid.

·         Possible excitotoxicity suggests findings of increased glutamine levels in the cerebrospinal fluid of patients with sporadic ALS.

·         Degenerative disorder of basal ganglia function that results in variable combinations of tremor, rigidity, and bradykinesia.

·         Characterized by progressive destruction of the nigrostriatal pathway, with subsequent reduction in striatal concentration of dopamine.

·         Idiopathic Parkinsonism – dopamine depletion results from degeneration of the dopamine nigrostriatal system

·         Postencephalitic syndrome as a side effect of therapy with antipsychotic drugs that block dopamine receptors, as a toxic reaction to a chemical agent, or as an outcome of severe carbon monoxide poisoning.

·         Deficiency of dopamine in the substantia nigra

·         Manifestations – tremor, rigidity, bradykinesia . tremor of the limbs, hands, feet, head, neck, face, lips, and tongue.

·         The pathophysiologic aspects of Alzheimer’s involve neuropathologic and neurotransmitter changes. It is characterized by cortical atrophy and loss of neurons, particularly in the parietal and temporal lobes. The ventricles are enlarged from loss of brain tissue. Microscopic features include neuritic plaques, neurofibrillary tangles, and amyloid agiopathy.

·         Amyloid Beta is the critical molecule in the pathogenesis of Alzheimer disease.

·         Plaques, tangles and associated neuronal loss and glial reaction are evident earliest in the emtorhinal cortex, then spread through the hippocampal formation and isocortex, and then extend to the neocortex.

·         Alzheimer has been associated with a decrease levels of choline acetyltransferase activity in the cortex and hippocampus. This enzyme is required for the synthesis of acetylcholine, a neurotransmitter that is associated with memory.

·         Alzheimer shows mutations in three genes- the APP gene on chromosome 21; presenilin-1, a gene on chromosome 14; presenilin-2, a gene on chromosome 1. The fourth gene, ApoE found on chromosome 19 increased the risk and lowers the age of onset.

·         Psychotic disorder of thought and language that is characterized by disorganized speech, delusions, visual and auditory hallucinations, and possible catatonic behavior. It affects a persons thoughts, feelings, perceptions and overall behavior while interfering with filtering of stimuli from the environment.

·         Brain dysfunction with alterations in anatomic structures, biochemical variations, and functional disturbances.  Not due to progressive brain deterioration or the effects of psychiatric medications but are caused by abnormalities in neurodevelopment that occur in prenatal or early postnatal life.

·         Enlargement of the lateral and third ventricles; reduction in frontal love, temporal love, and whole brain volumes; diminished neuronal content in both the thalamus and hippocampus.

·         Increased density of dopamine receptor sites, particularly in the basal ganglia. Decreased activity of serotonin, decreased activity of glutamate through dysfunction of its N-methyl-D-aspartate receptor. Norepinephrine and GABA have also been implicated in the patho of schizophrenia.

·         Delusions – false ideas believed by the affected person that cannot be corrected by reason

·         Hallucinations – present the end of the spectrum of increasing intensity of sensual stimuli.

·         Positive symptoms – delusions or false beliefs, hallucinations or abnormal sensory perceptions that occur without external visual or auditory input.

·         Negative symptoms reflect the absence of normal social and interpersonal relationships such as lack of motivation (alogia), apathy, and flattening of emotional expression.

·         Anxiety disorders are group of disorders that are characterized by intense episodes of fearfulness with symptoms related to activation of the sympathetic nervous system thorough the hypothalamic-pituitary-adrenal axis.

         Generalized anxiety disorder is characterized by excessive, uncontrollable worry. Characteristics include muscle tension, autonomic hyperactivity, and vigilance and scanning.

·         Obsessive-compulsive disorder is characterized by repetitive thoughts and actions. Behaviors such as hand washing, ordering, checking, praying, counting or repeating words must be repeated excessively and the repetition must not be related to any environmental condition. The person recognizes the unreasonable rituals. Dysfunction of the prefrontal cortex and structures of the basal ganglia, the caudate nucleus and globus pallidus. There is increased activity in the thalamus and the putamen of the basal ganglia and a decrease in serotonin. 

·         Panic disorder is characterized by an experience of intense fear with neurologic, cardiac, respiratory and psychological symptoms. Have a “fear network” that is centered in the amygdale and involves interactions with the hippocampus and prefrontal cortex. Projections from the amygdale to hypothalamic and brain stem sites account for many of the observed signs of the fear response. Manifestations include neurologic symptoms (dizziness, paretsthesias, fainting), cardiac symptoms (tachycardia, chest pain, and palpitations), respiratory symptoms (dyspnea), sweating, nausea or abdominal distress and psychological symptoms. First degree relatives of persons with panic disorder have 3- to 21- fold higher risks. Both biologic and environmental factors involved in panic attacks. Norepinephrine, serotonin, and GABA are the three neurotransmitters associated with this disorder and are often low. 

·         Social phobia is an intense fear reactions to social interaction

                                                   Head injury

                                              Closed head injury

                                                   Open head injury

–Head injury caused by impact. Examples: Contusions, lacerations, and hemorrhage.

– Head injury caused by brain swelling, infection, or cerebral hypoxia.

– Confined to one area of the brain; most often caused by open brain injuries but can be caused by closed as well.

                                            Brain contusion

– A bruise of a part of the brain. Just like any other soft tissue, the brain can sustain bruising when traumatized. As with any other bruise, small vessels are torn resulting in bleeding & swelling within the brain tissue. The damage caused by the contusion depends on where the head is impacted and the direction of the stress on the brain from the impact. As the skull receives the initial impact, it transfers the energy from the impact to the brain causing a contusion to form where the brain collides against the rough surface of the skull. The extent of the damage, as well as the effects of that damage, is dependent on the area of the brain that is injured. A contusion is a permanent injury. The effects of the injury are dependent upon where the contusion forms. If a contusion forms in a critical area needed to perform a specific function of the brain, such as a direct hit to the brain’s motor area, the injury wipes out any hope of recovering that function, in this case leaving the victim with permanent paralysis. There is also a chance that the contusion will not cause any alteration in the person’s ability to function normally, if it forms in an area of the brain that is not critical, or what is called a silent area. If the injury impacts the frontal lobe you are likely to have impaired thought processes or paralysis of the opposite side of the body. The Occipital lobe, on the other hand, is located in the back of the head and is responsible for all aspects of our visual capabilities. So, if a contusion were to form in the Occipital lobe, it would be probable that the victim could loose a half of their vision field in each eye.

Each area of the brain is responsible for a specific function of the human body. For example, parts of the frontal lobe (located in the front of the brain) are responsible for the ability to think and the ability to plan ahead. Other parts within the frontal lobe are devoted to motor capabilities; like the ability to move our eyes or head, orient our bodies and minds to what is going on around us, and move the opposite arm and leg. Neurons act as a communications network for the human nervous system.

The third possibility is if the contusion forms in an overlapping area of the brain. An overlapping area of the brain is one that is used to perform parts of more than one function. Because only part of the area needed to perform that function is gone, it is possible to re-learn the ability that was lost in the injury by re-routing the signals to areas of the brain not affected by the contusion. This means that although brain function is impaired, the patient may recover.

Symptoms depend on the extent of the brain contusion. A small contusion may not produce any visible symptoms if the damaged areas are not critical. The involvement of functional areas of the brain will produce varying degrees of impairment in:

•Thinking

•Reading and Writing

•Speech

•Memory

•Vision

•Coordination

If you experience a head injury it is always a good idea to have it looked at by a physician. It is also important to pay close attention to any changes or irregularities in your physical or mental capabilities after the incident and if they persist for any length of time to consult a physician. For example, if your vision is impaired, or you are having trouble manipulating a part of your body, like a leg or arm. Or if your speech is slowed, or thought process is cloudy

                                                 Coup brain injury

                                         Contracoup brain injury

                                           Epidural hematoma

– Hematoma lies beneath dura but on top of brain (“sub” = below”); Primarily venous bleeding with slower progression; can be acute, subacute, or chronic; most common on the top of the head but varies with location of blow to head; often bilateral; neurological deficits dependent on area of brain involved; onset time varies with type of subdural hematoma; chronic subdural hematomas are easily overlooked in people most at risk because there are no obvious signs or symptoms in the immediate period following the head injury.

Acute Subdural hematoma

– develop within hours

                                    Subacute Subdural hematoma

                                          Chronic Subdural hematoma

–develops over weeks to months; common after falls in the elderly, alcoholics, and patients on anticoagulants

                                               Intracerebral hematoma

                                                  Secondary Injury

                                                       Ischemia

                                                     Hypoxia

                                               Localized ischemia

– Example: stroke; manifestations will be seen depending on the location in the brain.

                                          Generalized ischemia

–Example: cardiovascular arrest; severe pathologic changes will result if this is not recognized quickly. The brain is unable to store energy with glucose and glycogen, so these are depleted quickly without adequate cerebral circulation. Depletion of these energy stores will occur in 4-5 minutes without restoration of circulation.

                              Increased Intracranial Pressure (IICP)

                                       Intracranial pressure (ICP)

Increased ICP compensation

                                                   Cushing reflex

                                    Central transtentorial herniation

                                               Uncal herniation

                                             Brain stem herniation

True or False

A chronic, debilitating psychotic disorder that involves the disconnection between thought and language is an accurate definition of schizophrenia.