Central Nervous System
The Brain |
Receives and processes sensory information, initiates responses, stores memories, and generates thoughts |
Spinal Cord |
Conducts signals to and from the brain, controls reflex activities. |
The Brain Structure
Cerebrum |
The largest part of the brain, made up of the cerebral cortex and other structures. The cerebrum is divided into two hemispheres. |
Cerebellum |
Coordinates movement by combining information from the eyes, ears, and muscles. |
Brainstem |
Connects the cerebrum and cerebellum to the spinal cord. The brainstem controls unconscious processes like sleep. |
The Brain Structure Visual
Divisions of the Brain
Forebrain |
Processes sensory information, helps with reasoning and problem-solving, and regulate autonomic, endocrine, and motor functions |
Midbrain |
Helps to regulate movement and process auditory and visual information |
Hindbrain |
Helps regulate automatic functions, relay sensory information, and maintain balance and equilibrium |
Divisions of the Brain Visual
The Limbic System
Limbic System |
(Primitive brain), regulates emotions (basic survival instincts), influences memories/learning, and motivation (basic drives). |
Thalamus |
Sensory relay center, receives input from all our senses except olfaction, critical in the perception of pain |
Hippocampus |
Stores memories, consolidation of conscious memories, stores new information and events as lasting memories |
Amygdala |
Processing fearful and threatening stimuli. Includes threat detection and activation of fear-related behaviors. |
Hypothalamus |
Maintains the body's homeostasis, (regulates temperature, hunger, thirst, sleep-wake cycle). Produces hormones that stimulate or inhibit the release of hormones from the pituitary gland. |
Corpus Callosum |
Connects the brain's left and right hemispheres, allowing them to communicate |
Basal Ganglia |
Motor learning, executive functions and coordination of movement, posture, inhibitory (allows us to be still) |
Olfactory Bulb |
is a part of the brain that processes smell |
Cingulate gyrus |
Involved in regulating emotions, processing pain, and regulating autonomic motor function. |
Pineal gland |
Helps control the circadian cycle of sleep and wakefulness by secreting melatonin. |
Suprachiasmatic Nucleus (SCN) |
Controls the body's circadian rhythms |
The Cerebral Cortex Visual
The Cerebral Cortex
Cerebral Cortex |
Involved in many high-level functions, such as reasoning, emotion, thought, memory, language and consciousness. |
Frontal Lobe: |
the largest portion of the brain (about ⅓ of the entire brain) divided into prefrontal cortex, premotor area, and motor area |
Parietal Lobe: |
Primary sensory areas that process somatosensory information, sensations of touch, pain, heat, and proprioception. |
Temporal Lobe: |
Auditory processing, memory information retrieval, and involved in emotional behavior. Connected to limbic system (hippocampus, amygdala, etc). |
Occipital Lobe: |
Visual perception, visual interpretation, and reading |
Frontal Lobe
Left Frontal Lobe: |
language, speech, and cognitive tasks. Includes broca's area |
Right Frontal Lobe: |
non-verbal communication (facial recognition) and environmental awareness |
Prefrontal Cortex (PFC) |
Integration center for all sensory information and executive functions (decision making, planning, working memory, personality expression, social behavior, speech and language). Personality center |
Broca's area |
Controls the muscles that produce speech and language comprehension |
Parietal Lobe
Left Parietal Lobe: |
Directing attention, visual & spatial skills |
Right Parietal Lobe: |
Motor routines and linguistic skills (reading, writing) |
Temporal Lobe
Left Temporal Lobe: |
Verbal memory and language comprehension. Includes wernicke’s area. |
Right Temporal Lobe: |
Visual memory |
Wernicke's Area |
Language comprehension = receives auditory signals from the ear and processes them to understand the meaning of spoken words |
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How does the SCN interact with the Pineal Gland? The SCN sends messages to the pineal gland, which triggers the release of melatonin at night and triggers the release of cortisol and other hormones to help you wake up in the morning.
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Peripheral Nervous System (PNS)
Somatic Nervous System: |
Sends and receives sensory messages that control voluntary motor movement of the skeletal muscles |
Automatic Nervous System: |
Controls automatic or involuntary bodily functions of the smooth muscles and glands |
Automatic Nervous System (ANS)
Primary Function: |
Maintain homeostasis (e.g., digestion, heart rate, & breathing) |
Sympathetic Nervous System (SNS) |
The Body's mobilizing system. Prepares the body for stressful or energetic activity (e.g., fight or flight) |
Parasympathetic Nervous System (PNS) |
Dominates during rest state, directs maintenance activities (e.g., rest and rumination) |
Sympathetic & Parasympathetic Effects
Myelination of the Vagus Nerve
Vagus Nerve |
A major nerve in the parasympathetic nervous system that helps regulate heart rate, digestion, and emotional responses. |
Myelination |
The process of covering nerve fibers with myelin, which improves the speed and efficiency of nerve signaling. |
Social Connection & Nervous System Development:
Safe Connection with Another Mammalian Nervous System:
This suggests that social interactions, particularly safe and supportive relationships, help stimulate and develop the vagus nerve.
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Brain Locus of Neurological Disorders
Type |
Disorders/ Description |
Locus of the Brain |
Movement disorders |
tics/OCD/tourettes |
Basal Ganglia |
Speech deficits |
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left frontal broca’s; left temporal Wernicke’s |
Sleep disorders |
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hypothalamus; pineal gland; SCN |
Memory |
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Wernicke's aphasia |
problems understanding speech |
left temporal lobe |
Broca's aphasia |
inability to express language |
left frontal lobe |
Brain Areas for Neurological Disorders
Delirium |
Alzheimer's Disease (AD) |
Parkinson's Disease |
Huntington's Disease (Chorea) |
Pseudodementia |
Major Frontotemporal Neurocognitive Disorder
Major Neurocognitive Disorder Due to HIV Infection
Neurocognitive Disorder due to Traumatic Brain Injury
Wernicke's Encephalopathy (WE)
Most often arises in people with AUD |
Symptoms: |
Paralysis of the eye muscles, ataxia, confusion |
Caused by thiamine deficiency (vitamin B1) |
Other causes: |
severe malnutrition, prolonged vomiting, extended IV nutrition, cancer, immunodeficiency, liver disease, hyperthyroidism, and severe anorexia. |
Risk: |
If left untreated, WE can lead to Korsakoff syndrome (KS) |
Wernicke-Korsakoff Syndrome
The disorder is associated with patients fabricating stories in the setting of clear consciousness. Confabulations can be spontaneous or provoked |
Cause: |
Severe brain disorder caused by a deficiency of thiamine (vitamin B1) |
Symptoms: |
Memory disturbances in which there are significant deficits in anterograde and retrograde memory |
Immediate memory is maintained, but short-term memory is diminished with intact sensorium.
Parkinson's
Features: |
Movement disorder with tremors, rigidity, bradykinesia, shuffling gait, and neuropsychiatric symptoms (e.g., depression, neurocognitive disorder). |
Brain Locus: |
Caused by the gradual loss of dopaminergic neurons in the Substantia Nigra (part of the Basal Ganglia, which regulates voluntary movement). |
Treatment & Psychopharmacology |
Levodopa (L-Dopa) - |
Dopamine precursor to improve movement |
Carbidopa - |
Reduces Levodopa side effects (e.g., nausea, hypotension) and enhances its effectiveness. |
Dopamine Agonists - |
Stimulate dopamine receptors |
Enzyme Inhibitors - |
MAO-B and COMT inhibitors slow dopamine breakdown. |
Amantadine - |
Helps reduce involuntary movements |
Anticholinergics - |
Reduce tremors and muscle rigidity |
Deep Brain Stimulation (DBS) - |
Surgical treatment for severe cases |
Alzheimer’s Disease (AD)
Definition: |
The most common major neurocognitive disorder (NCD), accounting for up to 80% of cases. |
Prevalence: |
Affects 1 in 8 people over 65, more common in women due to longer life expectancy. |
Neuropathology: |
Acetylcholine deficiency, affecting learning and memory; Amyloid plaques & neurofibrillary tangles; Damage to the hippocampus and amygdala |
Disease Progression: |
Begins up to 20 years before symptoms appear. 1: pre-clinical (no symptoms), 2: MCI, 3: dementia due to AD |
Symptoms |
Early: |
Memory loss, apathy, depression |
Progressive: |
Disorientation, confusion, impaired judgment, behavioral changes, motor and gait issues |
Late: |
Loss of communication, failure to recognize loved ones, bedridden |
Types of Dementia
Alzheimer's disease: |
The most common type, characterized by the accumulation of amyloid plaques and tau tangles in the brain |
Vascular dementia: |
Caused by damage to blood vessels in the brain, which reduces blood flow and oxygen to the brain |
Lewy body dementia: |
Characterized by the presence of abnormal protein deposits called Lewy bodies in the brain. |
Frontotemporal dementia: |
Affects the frontal and temporal lobes of the brain, leading to changes in behavior, personality, and language |
Mixed dementia: |
A combination of two or more types of dementia |
Dementia VS. Pseudo-dementia
Pseudodementia |
Cognitive impairment in older adults due to depression, mimicking a neurocognitive disorder (NCD). |
Key Differences |
Dementia (NCDs) |
Pseudodementia |
Progressive cognitive decline |
Slower processing speed, difficulty with concentration and attention, psychomotor retardation |
Patients often deny memory issues |
Patients acknowledge memory loss |
Irreversible deterioration |
Cognitive function improves once depression is treated |
Sleep Patterns Over the Lifespan
REM sleep decreases with age: |
Newborns: 50%; 5-year-olds: 20–25%; Older adults: 18% |
Functions of REM Sleep: |
Psychological restoration; Memory consolidation & emotional processing; Brain development; Dreaming (often bizarre and illogical) |
Movement Disorders
Originates in the: |
Basal Ganglia |
Definition: |
Abnormal repetitive movements |
Basal Ganglia: |
also the reservoir of our over-learned motor patterns, like riding a bike, automatic daily habits, backing out of the driveway, etc. |
Hyperkinetic |
Excess or involuntary movements (e.g., huntington’s disease/chorea, tremors, tics/ tourette's syndrome) |
Hypokinetic |
Slow or reduced movements (e.g., parkinson's disease, dementia with lewy bodies) |
Huntington's Chorea
Cause: |
Genetic disorder causing degeneration of basal ganglia neurons |
Symptoms: |
Choreiform (jerky, involuntary movements); Speech outbursts; Progressive cognitive decline |
Onset: |
Typically 40–50 years; often passed down before symptoms appear |
Treatment: |
No cure available |
Parkinson’s Disease
Cause: |
Damage to the Substantia Nigra, caudate nucleus, and putamen, dopamine-rich brain areas essential for movement and mood regulation |
Symptoms: |
Movement difficulties (tremors, rigidity, slowed initiation); Depression, psychosis in severe cases |
Possible Cause: |
Bacterial infections (e.g., from foodborne pathogens) may travel via the Vagus nerve, leading to inflammation and degeneration |
Prevalence: |
Increasing significantly (e.g., Michael J. Fox as a well-known case) |
Treatment |
L-Dopa (dopamine precursor) |
helps temporarily replenish dopamine and slow symptom progression |
Music Therapy |
may aid movement and mood regulation |
Tourette's Syndrome
Brain Area: |
basal ganglia, frontal lobes and cortex |
Comorbidities: |
OCD; ADHD; Anxiety |
Five A’s of Neurologic Symptoms
Ataxia |
Impaired coordination, balance, and speech |
Common Cause: |
Damage to the cerebellum or motor areas |
Apraxia |
Inability to perform skilled movements or gestures (e.g., difficulty winking) |
Common Cause: |
Parietal lobe damage |
Aphasia |
Impaired speech or language comprehension |
Types & Causes: |
Receptive aphasia; Expressive aphasia; Conduction aphasia |
Receptive Aphasia |
Damage to Wernicke’s area (left temporal lobe); speech is not understood |
Expressive Aphasia |
Damage to Broca’s area (posterior frontal lobe); difficulty producing speech |
Conduction Aphasia |
Damage to neural pathways connecting these areas, affecting verbal repetition |
Anomia |
Difficulty naming objects, people, or terms |
Common Cause: |
Likely damage to the hippocampus, thalamus, or other memory retrieval areas |
Agnosia |
Inability to recognize objects, people, or sensory stimuli |
Common Cause: |
Brain damage from strokes, injuries, dementia, or neurological disorders |
Subtype of Agnosia: |
Prosopagnosia ("Face Blindness") |
Prosopagnosia |
Difficulty recognizing faces |
Traumatic Brain Injuries & Concussions
External Trauma: |
Direct blow to the head, often blood vessels are torn so blood flow is blocked, tissue dies |
Internal Trauma: |
stroke (either clot or brain bleed) ,aneurysm, or brain tumor (internal trauma) |
Aftereffects of Head Trauma: |
Can cause memory impairments (post-traumatic amnesia, persistent memory deficits), executive functioning disturbances, and personality changes |
Phineas Gage Case (1848): |
The most well-known case of frontal lobe dysfunction. His injury led to drastic personality changes, later associated with "frontotemporal dementia." |
Aftereffects of Concussions: |
May result in a short-term loss of consciousness, anterograde amnesia (difficulty forming new memories), and retrograde amnesia (loss of past memories) |
Common symptoms: |
Dizziness, headache, fatigue; Difficulty concentrating, memory deficits; Irritability, anxiety, insomnia; Heightened sensitivity to noise and light; Hypochondriacal concerns |
Location of Brain Trauma & it's Impact
Aphasia: |
Loss of Speech or Language Comprehension |
Receptive Aphasia (Wernicke’s Aphasia): |
Damage to the left temporal lobe (Wernicke’s area) impairs language comprehension. The person may speak in gibberish but remain unaware of their incoherence. Temporal lobe damage can also affect semantic and long-term memory. |
Expressive Aphasia (Broca’s Aphasia): |
Damage to the posterior frontal lobe (Broca’s area) affects speech production. The person understands language and knows what they want to say but struggles to verbalize it, causing frustration. |
Conduction Aphasia: |
Damage to the neural pathways connecting Wernicke’s & Broca’s areas disrupts communication between comprehension and speech production. The person cannot effectively repeat verbal phrases. |
Global Aphasia: |
Widespread damage affecting both comprehension and speech production, severely impairing communication. |
Current Neuro-Imaging Options
PET Scan: |
Quick, cost-effective images of basic structures, very useful as first-line assessment in emergencies to identify brain issues that need emergent care (brain bleeds, etc). Uses radio |
MRI: |
More expensive, detailed images possible with enhanced soft-tissue resolution to pick up more subtle structural issues. Uses magnetic resonance |
CT Scan: |
Detailed metabolic picture of brain function. Can give info about low (Alzheimer's, stroke/blood vessel damaging affecting function) or high (brain tumor or other inflammatory or cancer-related process). Uses radioactive dye |
Memory/Types of Amnesia
Retrograde Amnesia: |
Occurs after head trauma, such as a blow to the head. The person cannot recall events leading up to the injury, sometimes spanning weeks or months before the event. However, the ability to form new memories remains intact. |
Anterograde Amnesia |
Seen in conditions like Alzheimer’s disease, where working memory fails, preventing the formation of new memories. The person struggles to learn new information, making daily functioning difficult. Remote (long-term) memory, particularly music memory, is often preserved. Linked to damage in memory-related brain structures, such as the hippocampus. |
Psychogenic Amnesia |
Caused by psychological factors rather than physical brain damage. Follows different patterns from neurological disorders. Short-term memory and the ability to form new memories remain intact. Long-term autobiographical memory is affected, leading to loss of personal details (e.g., name, birthdate). Unlike neurological amnesia, where long-term memory tends to be retained. |
Psychogenic Amnesia /(Psych) = Only one that long-term is affected
Differentiate Types of Seizures
Types of Seizures: |
Generalized & Focal Seizures |
Generalized Seizures (Gran & Petit Mal): |
Affect both hemispheres of the brain from the start and often cause loss of consciousness. (grand mal & petit mal) |
Gran Mal: |
Sudden loss of consciousness and stiffening (tonic activity), followed by clonic activity (rhythmic jerking). Most well-known type. |
Petit Mal: |
Brief episodes of staring, often mistaken for daydreaming. Occur most frequently in children. Last 0-30 sec |
Focal Seizures (Partial Seizures): |
Originate in a specific area of one hemisphere of the brain. They may or may not cause loss of awareness. (simple partial & complex partial) |
Simple Partial: |
Person remains conscious and aware. Characterized by abnormal movements that begin in one group of muscles and progress to adjacent groups of muscles in a slow wave of seizure activity per location in the back of the frontal lobe motor area. |
Complex Partial: |
Person has impaired consciousness or awareness. May involve staring, repetitive movements (lip-smacking, hand rubbing), or confusion. The person may not remember the seizure after it ends. Often a manifestation of temporal lobe epilepsy |
Next Two Are Focal Seizures |
Jacksonian Seizure: |
A type of focal seizure that originates in the primary motor cortex of the brain (part of the frontal lobe) and progresses in a characteristic pattern. Begins with localized muscle twitching (jerking movements) in a small part of the body, such as a finger, toe, or corner of the mouth. Spreads gradually to larger areas of the body (e.g., from hand → arm → face). |
Temporal Lobe Epilepsy (TLE) |
A type of focal seizure. Originate in the temporal lobes of the brain. Common Symptoms Before: Déjà vu. Can turn into tonic-clonic (grand mal) seizure. |
Neurotransmitter Functions & Effects
Neurotransmitter |
Behaviors or Diseases Related |
Acetylcholine (ACh) |
Learning and memory; Alzheimer's Disease's muscle movement in the peripheral nervous system. + ACh = spasms. - ACh = paralysis |
Dopamine (DA) |
Reward circuits; Motor circuits involved in Parkinson's disease; Schizophrenia |
Norepinephrine (NE) |
Arousal; Depression |
Serotonin (5HT) |
Depression, Aggression; Schizophrenia behavior. |
GABA |
Anxiety disorders, Epilepsy; Major inhibitory neurotransmitter in the brain |
Glutamate |
Learning; Major excitatory neurotransmitter in the brain |
Endogenous Opioids |
Pain; Analgesia (inability to feel pain); Reward |
KEY TERMS:
Mania: arousal, aggression
ADHD: learning, memory
Addiction: reward
Specific Disorders & Neurotransmitters
Alzheimer's disease |
Acetylcholine, due to it's role in the development of memory of the hippocampus |
(Repetitive) Movement disorders |
dopamine, due to it's role in movement |
Depression |
Low serotonin and low norepinephrine |
Mania |
Low serotonin and high norepinephrine |
Anxiety |
Too little GABA. |
Schizophrenia |
Excess dopamine; GABA & Glutamate imbalance |
Autism |
Too much serotonin; GABA & Glutamate imbalance |
Substance use disorder |
(Repetitive) Movement disorders: Parkinsons, tics, OCD
Glutamate and GABA
Maintain a homeostatic balance |
Glutamate & GABA have a seesaw relationship |
When glutamate is high, GABA is low |
Children with autism and related disorders tend to lean towards excess glutamate and low GABA |
Balance must be maintained for their bodies and nervous system to function properly |
Excessive Levels of Glutamate: Can lead to excitotoxicity (overstimulation of neurons), contributing to neurodegenerative diseases (e.g., Alzheimer’s, epilepsy, anxiety, stroke). |
Deficiency in GABA: Can lead to excessive excitability, associated with anxiety, seizures, and insomnia. |
Excessive Levels of GABA: Sedation, cognitive slowing, motor impairments. |
Disorders Related to this Imbalance: Epilepsy (excess excitation, insufficient inhibition). Schizophrenia (dysfunction in both systems). Anxiety disorders (GABA deficiency). |
Glutamate and GABA
Maintain a homeostatic balance |
Glutamate & GABA have a seesaw relationship |
When glutamate is high, GABA is low |
Children with autism and related disorders tend to lean towards excess glutamate and low GABA |
Balance must be maintained for their bodies and nervous system to function properly |
Excessive Levels of Glutamate: Can lead to excitotoxicity (overstimulation of neurons), contributing to neurodegenerative diseases (e.g., Alzheimer’s, epilepsy, anxiety, stroke). |
Deficiency in GABA: Can lead to excessive excitability, associated with anxiety, seizures, and insomnia. |
Excessive Levels of GABA: Sedation, cognitive slowing, motor impairments. |
Disorders Related to this Imbalance: Epilepsy (excess excitation, insufficient inhibition). Schizophrenia (dysfunction in both systems). Anxiety disorders (GABA deficiency). |
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Depression
Impact on the Brain: |
Can lead to brain shrinkage |
Neurotransmitter Imbalances: |
Serotonin, dopamine, and norepinephrine. All of which are interconnected |
Glutamate: |
Profoundly out of balance |
Treatment: Mild to Moderate Depression |
Regular exercise can be as effective as antidepressants; Psychotherapy (CBT) to help address negative thought patterns |
Treatment: Moderate to Severe Depression |
Antidepressant medications may be necessary, though it can take time to find the right one. Side effects (e.g., sexual dysfunction, weight gain, emotional blunting) can be a challenge |
Treatment: Electroconvulsive Therapy (ECT): |
Used for severe or treatment-resistant depression, particularly when rapid symptom relief is needed (e.g., in cases of suicidality or catatonia). |
Emerging & Alternative Options |
Ketamine therapy: |
Research suggests it may rapidly reduce depressive symptoms, particularly in treatment-resistant cases |
Transcranial Magnetic Stimulation (TMS): |
A non-invasive treatment using magnetic pulses, effective for depression, OCD, and other conditions. |
Bipolar Disorder: Tx & Considerations
Mood Stabilizers: |
Used to manage mood swings in bipolar disorder, preventing both manic and depressive episodes |
Common Meds: |
Lithium; anticonvulsants (e.g., valproate & lamotrigine); atypical antipsychotics |
Electroconvulsive Therapy (ECT) |
Typically used for severe cases of bipolar disorder or treatment-resistant depression; Involves brief electrical stimulation of the brain while the patient is under anesthesia. Effective for acute mood episodes but usually considered after medication and therapy have failed. |
Psychotic Disorders
Medications that block dopamine can help reduce psychotic symptoms, particularly hallucinations and disorganized thinking, known as "positive" symptoms of psychotic disorders |
However, "negative" symptoms (e.g., apathy, low motivation, and reduced activity) may be less responsive to treatment |
Due to side effects, medication adherence is often a challenge for individuals with psychotic disorders |
ECT Treatment
ECT involves a brief electrical stimulation of the brain while the patient is under anesthesia |
Used in patients with severe major depression or bipolar disorder that has not responded to other treatments |
Side effects: |
Memory loss (retrograde amnesia) is a significant concern; Patients may experience gaps in memory from weeks to months before treatment; If ECT is repeated over time, cumulative memory loss can become disruptive |
retrograde amnesia - an individual is unable to recall events that occurred before the onset of brain injury/ trauma, but ability to form new memories is intact.
Antidepressants Classes
Drug Class |
Function |
SSRIs |
Blocks reuptake of serotonin from space between neurons |
SNRI |
Block serotonin & norepinephrine reuptake |
NDRI |
Block reuptake of norepinephrine & dopamine |
TCAs |
Tricyclic antidepressants affects serotonin & norepinephrine |
MAOIs |
Block recycling of serotonin, norepinephrine, & dopamine |
Others |
Affect serotonin/ norepinephrine in other ways |
SSRI Danger Warnings
Increased Youth Suicide Risk |
Serotonin Syndrom |
Neuroleptic Malignant Syndrome |
Risk with Anticholinergic Agents
Seniors: |
Anticholinergic agents interact with many common medications taken by older people |
Risk of dementia: |
Increased risk of dementia in people who used them for longer than a few months |
Movement/Memory Medications
Neuroleptic Medications Side Effects
Serotonin Syndrome
Mild |
Moderate |
Life Threatening |
Mydriasis (dilated pupils) |
Altered Mental Status (e.g., agitation, disorientation, excitement) |
Delirium |
Shivering/Sweating |
Autonomic Hyperactivity (e.g., rigidity, tachycardia, hyperthermia) |
Hypertension/ Hyperthermia |
Tachycardia (mild) |
Neuromuscular Abnormalities (e.g., tremor, clonus, hyperreflexia) |
Muscle rigidity/ Tachycardia |
Management Stages: |
Observe for at least 6 hrs |
Admit to hospital; Cardiac monitoring |
Intensive Care Unit; cooling meaures |
Benzodiazepines |
Cyproheptadine |
Sedation; SkM paralysis; ventilation |
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