Clinical Script for Ischemic Stroke/TIA - PDF

Clinical Script for Ischemic Stroke/ TIA (Transient Ischemic Attack) Brian Attack Lack of blood flow in a cerebral vessel causing brain ischemia Sudden onset of loss of neurological function Neurological symptoms are based on where the lack of blood flow occurs If symptoms are less than 24 hours- it is technically a TIA (although most TIAs are less than 1 hour). If symptoms are greater than 24 hours, it is considered a stroke It is important to know the “last known well” in the clinical history to assist in determining tpA (tissue plasminogen activator) candidacy Strokes can be large vessel or small vessel Large vessel strokes include strokes occluding the ICA, MCA, ACA, PCA, basilar or vertebrals Small vessel strokes are typically pontine, basal ganglia and thalamic perforators or small distal branches of the main vessels. The risk factors for stroke include atrial fibrillation (embolic), greater than 70% stenosis of the internal carotid artery (thrombotic and/or arterial to arterial embolic), hypertension, diabetes Type I or Type II, hypercholesterolemia, tobacco abuse and obstructive sleep apnea. Patients who are having acute stroke symptoms, have no exclusion criteria for tpA (no intracranial bleeding, no use of anticoagulants with therapeutic lab values or timelines since last dose, no bps over 185/110 that cannot be controlled with intravenous antihypertensives, no stroke in the last three months), and can receive the medication in less than three hours from time of onset of symptoms- should receive tpA after discussion with the patient and/or family once they have a head CT without contrast that shows no contraindications (no masses or bleeding). o Special consideration is given to patients who present within the 3-4.5 hour time window for tpA administration. There is a 6% bleeding rate with tpA: of that 6%: 3% are asymptomatic; 2% are symptomatic and cause clinical worsening and 1% are fatal. Those who receive tpA need to be in an intensive care unit overnight and be in a hospital where neurosurgery is readily available If the patient is found to have a large vessel occlusion, they may be a candidate for interventional thrombectomy. All patients with a stroke and/or TIA need a risk factor assessment: telemetry monitoring for paroxysmal atrial fibrillation; cerebrovascular imaging; Echocardiogram with bubble study (for patent foramen ovale); Hemoglobin A1C; cholesterol panel and blood pressure monitoring as well as tobacco use history and assessment for obstructive sleep apnea. All abnormal risk factors must be addressed to prevent further strokes: if there is atrial fibrillation the patient will most likely be started on anticoagulation- warfarin or a DOAC medication; if there is greater than 70% stenosis of the internal carotid artery surgery or stenting may need to occur. The remainder of patients will be put on either aspirin, clopidogrel (Plavix), or both. Patients will be assessed by speech therapy, occupational therapy, and physical therapy All patients with acute symptoms of stroke should be encouraged to call 911 immediately. “Time is brain”. Strokes recover slowly- younger patients and those with minimal secondary health issues will do better. Acute aggressive inpatient therapy achieves improved outcomes. Ongoing therapy can lead to improved outcomes. Rule of thumb- what the stroke patient still has in terms of deficits at the one-year anniversary of stroke, is what will remain with them long term Major differentiators of strokes: o Left MCA- aphasia with right hemiparesis involving face and arm more than the leg o Right MCA- left sided neglect and left hemiparesis and sensory neglect o ACA strokes- contralateral leg weakness (can get some arm weakness) o PCA stroke (bilateral)- cortical blindness- thinks they are seeing things but are not- o PCA (unilateral)- homonymous hemianopsia contralateral o Brainstem strokes- the “Ds”- diplopia, dizziness, dysphagia o Small vessel strokes- anterior limb int capsule- pure motor stroke; posterior limb int capsule- motor and sensory; thalamic stroke- pure sensory stroke Seizures- Clinical Scripts- by: Diana Greene-Chandos MD, Anish Deshmukh, MD, and Maryam Hosseini, MD Generalized Seizures: 1. Absence Seizures 2. Generalized Tonic-Clonic Seizures (aka Grand Mal) Focal Onset Seizures: 1. Focal Aware Seizures (FAS aka Simple Partial Seizures) (non-motor vs motor) 2. Focal Impaired Awareness Seizures (FIAS aka Complex Partial Seizures/Petit Mal) Psychogenic Non-Epileptic Seizures (PNES)- seen in conversion disorder (severe stress manifesting as a seizure without any EEG abnormalities during the “seizure”. Status Epilepticus- any seizures lasting greater than 5 min in time OR more than one seizure without full recovery in between Absence Seizures: Typical onset is ages 4-8 years. There is no aura (a warning sign that a seizure will start). There is a sudden, brief lapse of consciousness, with momentary blinking, staring, or small movements of the lips or hands, but no falling. Typical absence seizures last less than 10 seconds and stop abruptly, with a prompt return to normal. Atypical absence seizures may last more than 10 seconds; there may be a brief period (10-20 seconds) of confusion followed by a return to normal. Generalized Tonic-Clonic Seizures: The typical onset for seizures due to Epilepsy (two unprovoked seizures, 24hrs apart, not due to an underlying medical condition like hypoglycemia)- is late childhood/early adolescent. The person loses consciousness suddenly, sometimes with a cry, and the body stiffens into tonic extensor rigidity. Breathing stops, and the patient can become cyanotic (blue color due to low oxygen saturations). A clonic phase happens next with rhythmic muscular contraction. Breathing resumes and is often noisy with excessive salivation. Injury, tongue biting, and urinary incontinence may occur. Post-ictal (after seizure), the patient may be confused, drowsy, fatigued, have a headache, muscular aching, and sometimes can have temporary weakness of one side of the body that resolves (called Todd’ paralysis). The person has full amnesia of the seizure event. Focal Aware (aka Simple Partial) Seizures The common theme is no loss of consciousness with focal aware seizure- the patient is fully awake and alert during the event. Focal Aware Seizures (non-motor) Can occur at any age. No aura. o (sensory) Seizures can be a tingling sensation on one side of the body or one limb. Or can be olfactory hallucinations lasting a few minutes (smell of burning metal), or auditory (buzzing noise, hearing music) or visual (flashing lights). These seizures can last 30 seconds to multiple min. When they stop, the person returns to normal. o (Autonomic) No aura (although some consider this focal aware seizure an aura itself before a generalized tonic-clonic seizure [so focal onset seizure that converts into a generalized seizure] OR evolution into a focal impaired awareness seizure. This sensation involving the autonomic nervous system can give the following symptoms: an epigastric “rising” (the sensation you get when an elevator abruptly goes up), nausea, pallor, flushing, and lightheadedness. o (emotional) Anxiety or fear, feeling of familiarity (déjà vu), feeling of unreality (Alice in Wonderland), fear or rage reactions, flashback experiences, and more complex hallucinations. This can also be an aura before a generalized or focal impaired awareness seizure. Focal Aware Seizure: Motor- No aura. Seizure is tonic then clonic that starts unilaterally in the hand, foot, or face. If there is spread to the other body parts on the same side, this is known as “Jacksonian March”. Typically lasts 30-60 sec. There can be post-seizure weakness temporarily on that side, but otherwise, the patient returns to normal. Focal Impaired Awareness Seizure (FIAS aka Complex Partial Seizures/Petit Mal): These seizures can start in childhood (typically around age 9) but also in adulthood. They are the most common type of seizure in adults. This seizure may start with autonomic or psychic phenomenon (“aura”). Consciousness is impaired, and the person appears confused. Automatisms include automatic motor behaviors such as checking, smacking the lips, walking about and unbuttoning or picking at clothes. Seizures usually last about 1-2 minutes. The patient may remember the initial symptoms (or “aura”) but is amnestic for the rest of the seizure. Temporary confusion and headache may occur after the seizure. Provoked Seizures Seizures can occur due to a toxic or metabolic abnormality. Below are the most common etiologies Hypoglycemia Extreme Hyperglycemia (blood glucose over 600) Hyponatremia Hypocalcemia Uremia Viral encephalitis Meningitis of all etiologies Withdrawal of alcohol Withdrawal of benzodiazepine medications Withdrawal of barbiturate medications Methamphetamines Pre-Eclampsia Febrile (in children) Certain medications (buproprion) Autoimmune-mediated encephalitis (like anti-NMDA encephalitis) These seizures do not constitute Epilepsy since reversing the trigger of the seizure (in a previously seizure- free patient) will remove the risk of further seizures. Otherwise, neurological injuries can cause seizures. Stroke where the cerebral cortex is injured Cerebral Abscesses Brain tumor (primary or metastatic) Intracerebral Hemorrhage Subarachnoid Hemorrhage Subdural Hematoma Traumatic Brain Injury Diffuse hypoxic-ischemic encephalopathy Seizures can be due to congenital malformation and due to genetic syndromes. There are many anti-convulsant medications. The newer medications have fewer side effects and do not require blood monitoring like the older medications. Electroencephalogram testing or longer-term recordings can be helpful in identifying where the seizures originate (if they start as focal seizures). Longer-term monitoring is useful to see how seizure evolves. Plus, it can also diagnose and identify the type of seizures seen mostly in critically ill patients called non- convulsive status epilepticus. In some circumstances, surgery is used to decrease seizures. This is mostly so with Focal onset seizures originating from the hippocampus (causing something called mesial temporal sclerosis- where the hippocampus is scarred and becomes smaller). MRI brain can help diagnose it. If the EEG and MRI both show the majority of the seizures coming from one side, and medications are failing to control the seizures, then a partial temporal lobectomy can be performed. Typically, this is an awake procedure (waking up the patient after the skull and meninges are opened). Then, the surgeon will map where language and short-term memory are intraoperatively to avoid any injury to those areas. Successful removal of the seizure focus can dramatically reduce the number of seizures if not curative at times. Clinical Scripts for Headache Types Migraine Headaches 80% have positive family history Female to male ratio is 3:1 Classically unilateral (60%) and throbbing/pounding in quality 15% have an aura- with visual changes, scotoma (blind spots) or scintillating scotoma (squiggly or jagged lines with flashing lights) Associated with photophobia (light sensitivity) and phonophobia (sound sensitivity) Associated with nausea and occasional vomiting Can be triggered by stress, odors, certain foods (chocolate, certain cheeses), alcohol (particularly red wine), menstruation and sleep deprivation. Improves with rest/sleep in a quiet and dark room- activity make it worse Treatment has two tiers: prophylactic and acute Prophylactic treatment includes daily medications with beta blockers, calcium channel blocker, certain anticonvulsants, and anti-depressants in addition to dietary and lifestyle changes Acute treatment is for acute headaches: ibuprofen, triptans, anti-emetics Tension Headaches Usually in men and women in their 20s-50s The most common type of headache Bilateral, band-like and dull/squeezing in quality Late afternoon timing typically Worse with stress and sleep deprivation Can be associated with TMJ (temporal mandibular joint syndrome) Activity does not make it worse Chronic tension headaches can be associated with depression Treatment with NSAIDS or acetaminophen/ sleep hygiene/ assessment for depression/TMJ/ Posture dysfunction Cluster Headaches Male to female ratio is 6:1 Mean age of onset is in 30s Unilateral very severe, stabbing peri-/retro-orbital lasting 15 min to 3 hours Seasonal Attacks occur in series (up to six attacks a day/ daily for weeks), followed by months of remission Often wakes patient up within ninety minutes of onset of sleep Associated with ipsilateral lacrimation (85%), ptosis, nasal congestion and rhinorrhea Acute treatment can be with 100% oxygen or a triptan Prophylaxis with verapamil (calcium channel blocker), lithium or anticonvulsants Temporal Mandibular Joint Disorders Can be related to previous jaw or facial trauma; osteoarthritis These are medical and dental conditions affecting either the joint itself or the muscles of mastication Symptoms include: headache, chronic ear pain, jaw stiffness, facial pain, pain with chewing, jaw joint noises, and grinding (Bruxism) or clenching one’s teeth. Treatment options inclue: o NSAIDs/relaxation techniques/stress reduction o Muscle relaxants o Dental appliance (mouth guard) o Provide muscle relaxation and support for the jaw joints (TMJ) o Refer to dental/oral surgery Temporal Arteritis Female to male ratio of 2:1 Age greater than 50 years Unilateral temporal headache Associated with jaw claudication, temporal artery tenderness with palpation, ESR (sedimentation rate) greater than 50. 50% also have symptoms of polymyalgia rheumatica (painful muscles in the neck, shoulders and upper back) If not treated can lead to blindness Screen by obtaining ESR and diagnose with temporal artery biopsy Start corticosteroid (prednisone) treatment as soon as suspected to prevent blindness Never delay treatment while awaiting confirmatory biopsy results Medication Overuse Headaches Headache occurring on 15 or more days/month in a patient with a pre-existing primary headache Developing as a consequence of regular overuse of acute or symptomatic headache medication (on 10 or more or 15 or more days/month, depending on the medication) for more than 3 months. It usually, but not invariably, resolves after the overuse is stopped. Clinical Scripts- Neuro/Psych Correlate From Bates, Guide to Physical Examination and History Taking, 11 th edition Depression- roughly 15 million Americans have major depression, and these often co-exist with anxiety and substance abuse. Depression is twice as common in women and is a frequent companion of chronic medical illness. The prevalence of post-partum depression is 10-15%. It is recommended to screen high-risk patients for early signs of depressive that are often missed: low self-esteem, loss of pleasure in daily activities (andedonia), sleep disorders, and difficulties concentrating or making decisions. Watch even more for depressive symptoms, in vulnerable patients like those who are young, female, single, divorced or separated, seriously or chronically ill, bereaved or have other psychiatric disorders, including substance abuse. Prior history or family history of depression also place patients at risk. However, note that risk factors alone are not sufficient to identify patients who are depressed. Failure to diagnose depression can have fatal consequences- suicide rates among patients with major depression are eight times higher than in the general population. Major Depressive Episode- At least five of the symptoms listed below (including one of the first two) must be present during the same two-week period. They must also represent a change from the person’s previous state. Depressed mood (may be an irritable mood in children and adolescents) most of the day, nearly every day. Markedly diminished interest or pleasure in almost all activities most of the day, nearly every day Significant weight gain or loss (not dieting) or increased or decreased appetite nearly every day Insomnia or hypersomnia nearly every day Psychomotor agitation or retardation nearly every day, Fatigue or loss or loss of energy nearly every day. Feelings of worthlessness or inappropriate guilt nearly every day Inability to think or concentrate or indecisiveness nearly every day Recurrent thoughts of death or suicide, or a specific plan for or attempt at suicide. The symptoms cause significant distress or impair social, occupational, or other important functions. In severe cases, hallucinations and delusion may occur. Dysthymic Disorder- A depressed mood and symptoms for most of the day, for more days than not, over the last two years (one year in children and adolescents). Freedom from symptoms lasts no more than two months at a time. Manic Episode- This is a distinct period of abnormally and persistently elevated, expansive, or irritable mood must be present for at least a week (any duration if hospitalization is necessary). During this time, at least three of the symptoms listed below have been persistent and significant. (Four of these symptoms are required if the mood is only irritable). Inflated self-esteem or grandiosity Decreased need for sleep (feels rested after sleeping 3 hours) More talkative than usual or pressure to keep talking Flight of ideas or racing thoughts Distractibility Increased goal-directed activity (either socially, at work or school, or sexually) or psychomotor agitation Excessive involvement in pleasurable high-risk activities (buying sprees, foolish business ventures, sexual indiscretions) The disturbance is severe enough to impair social or occupational functions or relationships. It may necessitate hospitalization for the protection of self or others. In severe cases, hallucinations and delusions may occur. Hypomanic Episode- The mood and symptoms resemble those in a manic episode but are less impairing, do not require hospitalization, do not include hallucinations or delusions, and have a shorter minimum duration- 4 days. Anxiety Disorders These are the anxiety disorders seen, but we will focus on generalized anxiety disorder. The other anxiety disorders are: panic disorder, agoraphobia, specific phobia, social phobia, obsessive-compulsive disorder, acute stress disorder, post-traumatic stress disorder. Generalized Anxiety Disorder- This disorder lacks a specific traumatic event or focus for concern. Excessive anxiety and worry, which the person finds hard to control, are about a number of events or activities. At least three of the following symptoms are associated: Feeling restless, keyed up, or on the edge Being easily fatigued Having difficulty in concentrating or having the mind going blank Irritability Muscle tension Difficulty in falling or staying asleep, or restless unsatisfying sleep. The disturbance causes significant distress or impairs social, occupational, or other important functions. Psychotic Disorders- These disorders involve grossly impaired reality testing. Specific diagnoses depend on the nature and duration of the symptoms and on a cause when it can be identified. Schizophrenia will be focused on for this document. Schizophrenia- Impairs major functioning, as to work or school or in interpersonal relations or self-care. For this diagnosis, performance of one or more of these functions must have decreased for a significant time to a level markedly below prior achievement. In addition, the person must manifest at least two of the following for a significant part of 1 month: Delusions Hallucinations Disorganized Speech Grossly disorganized or catatonic behavior Negative symptoms such as a flat affect, alogia (lack of content in speech), or avolition (Lack of interest, drive, and ability to set and pursue goals). Continuous signs of the disturbance must persist for at least six months. Dementia- an “acquired syndrome of decline in memory and at least one other cognitive domain such as language, visuospatial, or executive function sufficient to interfere with social or occupational functioning in an alert person.” Alzheimer’s Disease the most common form of dementia, affect 13% of Americans over the age of 65. As the again population increases, by 2050 prevalence will exceed 13 million cases. Risk factors include advancing age, family history and the gene mutation apolipoprotein E4. Risk of AD more than doubles in first degree relatives. Risk doubles in the presence of one APO E4 allele and increases fivefold or more in the presence of two alleles. Features on exam: normal alertness but progressive global deterioration of cognition in multiple domains, including short-term memory, but with sparing of memory for remote events; subtle language errors; visuospatial perception difficulties; and changes in executive function, or the ability to perform sequential tasks such as independent activities of daily living. Memory difficulties may take the form of repeating questions, losing objects, forgetting to pay bills, getting lost or confusion when performing tasks such as shopping. Later stages include impaired judgement and disorientation progressing to aphasia, apraxia, left-right confusion and ultimately dependence of IADLs. Psychosis and agitation may also occur. Mild Cognitive Impairment- Evidence of memory impairment without cognitive deficits or functional decline. There is a greater risk of developing Alzheimer’s Disease (AD) with MCI, progressing to AD at a rate of approximately 12-15% per year. D2A High Yield Notes Safe Opioid prescribing November 22, 2021 I. Epidemiology of the Opioid Epidemic 20% of the US adult population (50 mill) have chronic pain 3-4% of the US adult population is on chronic opioids 21-29% of patients prescribed opioids misuse them 8-12 % of patients using an opioid for chronic pain develop an Opioid Use Disorder The prevalence of opioid use disorder is 1.6 million. The current opioid epidemic began in 1999 From April ‘20 to April ’21 close to 100,000 people died of drug overdose in the U.S. II. Evidence for efficacy of opioid medications There is evidence for efficacy of short-term (12 weeks of less) therapy with opioid medication; Patients on chronic opioid medication report relief of pain in surveys; There is little evidence to support the efficacy of long term opioid use for treatment of chronic pain. III. CDC Guidelines1: 12 recommendations 1. Nonpharmacologic and nonopioid therapy is preferred for chronic pain (outside of active cancer, palliative or end-of-life care.) 2. Establish goals for pain and function. Continue opioid therapy only if there is a clinically meaningful improvement in pain and function that outweighs the risk. 3. Discuss the risk and benefits of therapy with patient before starting therapy and periodically during treatment. 4. Use immediate-release opioids when starting rather than extended-release or long-acting opioids. 5. Use the lowest possible effective dosage to reduce risks of opioid use disorder and overdose. 6. Prescribe opioids for short durations for acute pain to reduce the risks of opioid use disorder. 3-7 days will often be sufficient. 7. Evaluate the benefits and harms frequently, beginning 1 to 4 weeks after starting therapy. 8. Use strategies to mitigate risk, such as prescribing naloxone. 1Dowell D, Haegerich TM, Chou R. CDC Guideline for Prescribing Opioids for Chronic Pain— United States, 2016. JAMA. 2016;315(15):1624–1645. doi:10.1001/jama.2016.1464 9. Review PMP data. Monitor patients use of controlled substance using state prescription drug monitoring program. 10. Use urine drug testing before starting therapy and at least annually thereafter. 11. Avoid concurrent opioid and benzodiazepine use when possible. 12. Offer treatment for opioid use disorder. If a patient develops an opioid use disorder while on therapy, refer the patient for treatment with Medical-Assisted Treatment. IV. New Mexico state legal requirements for prescribing opioids Educate the patient about the risks of overdose Establish a controlled medication contract Check urine toxicology every 6 months Check NM PMP before prescribing and every 3 months while on medication Prescribe Narcan and provide written education about its use. V. Best practices of IPE Communication 2 Communicate respectfully, openly, and without bias, with a patient-centered focus. Establish rapport and build trusting relationships. Embrace and appreciate the roles and responsibilities of other health care professionals. Show empathetic behaviors for the patient and other health care professionals that include avoidance of stigma. Actively engage in finding solutions and resolving conflict. 2Interprofessional Education Collaborative and Owen JA, Skelton, JB, Miller WA, Moon JY, and Romanelli F (unpublished data, 2020). High Yield Notes/Clinical Script to Cerebral Cavernous Malformations Cerebral cavernous malformations are collections of small blood vessels (capillaries) are enlarged and irregular in structure. These capillaries have abnormally thin walls, and they lack other support tissues, such as elastic fibers, which normally make them stretchy. As a result, the blood vessels are prone to leakage, which can cause the health problems related to this condition. Cavernous malformations can occur anywhere in the body, but usually produce serious signs and symptoms only when they occur in the brain and spinal cord (which are described as cerebral). Approximately 25% of individuals with cerebral cavernous malformations never experience any related health problems. Other people with this condition may experience serious signs and symptoms such as headaches, seizures, paralysis, hearing or vision loss, and bleeding in the brain (cerebral hemorrhage). Severe brain hemorrhages can result in death but this is rare. The location and number of cerebral cavernous malformations determine the severity of this disorder. These malformations can change in size and number over time. Brainstem cavernous malformations are the most likely to bleed. Seizures are the #1 reason a person with CCM will come to the hospital with 50% of patients having a seizure who have these lesions. University of New Mexico is one of a small number of academic medical centers in the country who are an Angioma Centers of Excellence. The angioma alliance is a non-profit group that assists patients and families with the disease. Here is the link: https://www.alliancetocure.org There are two forms of the condition: familial and sporadic. The familial form is passed from parent to child, and affected individuals typically have multiple cerebral cavernous malformations. The sporadic form occurs in people with no family history of the disorder. These individuals typically have only one malformation. Northern New Mexico has the highest rate of prevalence of CCM and the genetic mutations. University of New Mexico is one a small number of academic medical center Mutations in at least three genes, KRIT1 (also known as CCM1), CCM2, and PDCD10 (also known as CCM3), cause familial cerebral cavernous malformations. The precise functions of these genes are not fully understood. Studies show that the proteins produced from these genes are found in the junctions connecting neighboring blood vessel cells. The proteins interact with each other as part of a complex that strengthens the interactions between cells and limits leakage from the blood vessels. Mutations in any of the three genes impair the function of the protein complex, resulting in weakened cell-to-cell junctions and increased leakage from vessels as seen in cerebral cavernous malformations. Mutations in these three genes account for 85 to 95 percent of all cases of familial cerebral cavernous malformations. The remaining 5 to 15 percent of cases may be due to mutations in unidentified genes or to other unknown causes. Mutations in the KRIT1, CCM2, and PDCD10 genes are not involved in sporadic cerebral cavernous malformations. The cause of this form of the condition is unknown. This condition has an which means one copy of the altered gene in each cell is sufficient to cause the disorder. In the familial form, an affected person inherits the mutation from one affected parent. Most people with cerebral cavernous malformations have the sporadic form of the disorder. These cases occur in people with no history of the disorder in their family and typically one results in one lesion. High Yield Notes- Guide to Clinical Skills: Comprehensive Neurologic Exam A. General Examination Observe posture, spontaneous movement, tics, fidgeting, abnormal muscle movements (twitches, fasciculation, jerking), brady-/hypokinesia, facial expression (e.g. flat facies of Parkinsonism), level of arousal and awareness of surroundings. Observe patterns of speaking, and volume of voice. Observe for eye contact and note if the patient is ill-appearing or in obvious pain. Please also perform any additional exam that may assist with etiology of the neurological issue such as carotid artery auscultation, heart auscultation, HEENT exam, cervical spine palpation and ROM, Lumbar spine palpation and ROM, Skin examination and peripheral vasculature pulse palpation. Note: The neuro exam can be challenging because it is largely dependent on the participation of the patient, particularly with descriptions of symptoms that cannot be observed, such as numbness or tingling1. Take extra care to not suggest (i.e. via miming) what symptoms you’re trying to elicit from the patient. Secondly, note the patient’s baseline. For example, many patients with diabetes have baseline peripheral neuropathy. Finally, it is important to ask the patient to give his/her own interpretation of the symptoms, because doing so can expose paranoia, anxiety, or even delusions that may be helpful in formulating a diagnosis1 (e.g. a common symptom in patients with dementia is paranoia, and psychosis is experienced by many patients with Huntington’s disease). B. Vital Signs During an examination, vital signs will be written on the door sign. In clinical practice, be aware of certain neurological diseases that can accompany changes in vital signs. (e.g. many patients with Parkinson’s disease experience postural hypotension; irregularly irregular heart rhythm (seen in atrial fibrillation) may be seen with transient ischemic attacks (TIA) or stroke. C. The Mental Status Examination You will NOT be expected to perform a detailed mental status exam in the depth detailed below when asked to do a neuro exam during a test. The items in red are items that you will do. The items in black below are for your information only to be used in real-life settings when circumstances dictate the need for more detailed mental status exam such as in the case of memory loss or dementia concerns. If you’re just studying for the neuro exam, skip this section. FOR YOUR NEURO EXAM AND EVERY NEURO EXAM WHERE MEMORY LOSS OR DEMENTIA CONCERNS ARE NOT PART OF THE COMPLAINTS Assess orientation by asking the four following questions: 1. “What is your full name?” (Orientation to self) 2. “What is the date today?” (Orientation to time) 3. “Where are you right now?” (Orientation to location) 4. “Why are you here?” (Orientation to situation) If a patient answers all four questions correctly, they are reported to be oriented x4. Brief assessment of language: 1. Naming- ask the patient to name three objects that you may be wearing by showing the item to the patients and asking “what is the name for this?” (ie watch, bracelet, stethoscope). Problems with naming if the patient is fully awake, alert and attentive suggests an expressive aphasia (Broca’s/non-fluent) OR part of a global aphasia. 2. Comprehension- this is often discovered through the interview and if they are able to respond appropriately to questions; however, to briefly, formally assess- ask the patient to “close their eyes” or to “take their right finger and touch their left ear”. Problems with language comprehension can usually be quickly discovered in the interview process; however, an inability to follow a command through language without showing them what to do suggests a receptive aphasia (Wernicke’s/fluent) OR part of a global aphasia. 3. Repetition- have the patient repeat a simple phrase- most usually use “Today is a sunny day”. If the patient cannot repeat a sentence this is called a conductive aphasia if naming and comprehension are intact. D. Cranial Nerves I (Olfactory): This nerve is usually not routinely tested except in specific situations, such as in patients experiencing acceleration/deceleration injuries, such as car accidents. In these injuries, the olfactory nerves passing through the cribriform plate of the ethmoid bone at the skull base may be sheared off, resulting in sudden loss of sense of smell. To test, use a strong-smelling substance, such as peppermint or clove oil, or coffee and have the patient manually close one nostril, then the other. Test each nostril individually II (Optic): 1. Assess visual acuity using a near card. Hold near card about 14 inches from the patient’s face while the patient covers one eye. Ask the patient to read the line with the smallest print possible. Repeat with opposite eye. Glasses are left on. 2. Assess visual fields in each eye separately. There are two different ways you can do this. First way: have patient cover their right eye with their right hand. You cover your right eye. Ask patient to fix their gaze on your nose. Using your left hand, hold different numbers of fingers at each of the four corners of your left field of vision and ask patient to tell you how many fingers you’re holding up. Repeat on the opposite side. Second way: Have patient cover right eye with right hand and fix their gaze on your nose. Close your right eye. In all 4 corners of your field of vision, wiggle your index finger up and down and ask patient if they can see the movement. Repeat on the opposite side. 3. Perform a fundoscopic exam in each eye. Do this after testing for visual acuity because the bright light of the fundoscope can temporarily blind people. II (Optic), III (Oculomotor): Assess pupillary function of each eye. Dim the room lights and use your pen light to assess pupillary function in each eye. Shine light into each eye at least twice, first looking at the pupillary function of the eye into which you’re shining the light and secondly, looking at pupillary function of the eye into which the light is not being shone (consensual pupillary constriction: both pupils should constrict equally when you shine a light into one eye III (Oculomotor), IV (Trochlear), VI (Abducens): Assess extraocular movements in 6 Note: Observe pupil size and reactivity to light, direct, consensual and during convergence, and the position of the eyelids. Optic tract fibers innervate both Edinger-Westphal nuclei, which control pupillary constriction and accommodation, thus, if there is a lesion in one optic nerve, a light stimulus in the affected eye will have no effect on the opposite pupil, although the ipsilateral pupil will still constrict1. This is called an afferent pupillary defect (Marcus Gunn pupil1. cardinal directions by having the patient follow your finger with their eyes. Observe for the presence of nystagmus at rest and at end gaze while assessing eye movements. https://radiopaedia.org/images/20994677 V. (Trigeminal): 1. Assess facial sensation to light touch bilaterally. Assess the three branches of the trigeminal nerve- ophthalmic, maxillary, and mandibular- by simultaneously lightly touching both sides of the patient’s forehead, cheeks, and chin. Ask patient to compare the sensation on both sides. 2. Check masseter contraction. Have patient bite down and simultaneously palpate the bilateral masseter muscles. Look for abnormalities in muscle tone and bulk. VII. (Facial): 1. Observe facial expression: Note any smoothness of the nasolabial folds. Ask patient to smile (if patient smiles with mouth closed, ask patient to “Show me all your teeth”). Observe symmetrical rise of the lips and deepening of the nasolabial folds (normal). 2. Check upper and lower face bilaterally: Ask patient to close eyes, squeeze them tight and don’t allow you to attempt to open them manually (gently). Ask patient to raise both eyebrows at the same time. Ask patient to puff out cheeks Note: Opening of the eyelids is controlled by the levator palpebrae (CN III) and superior tarsal/Muller muscles (sympathetic fibers). Closure of the eyelids is accomplished by the orbicularis oculi muscles (CN VII). These tests distinguish between central (e.g. stroke) and peripheral (e.g. Bell’s palsy) lesions of the facial nerve. In central facial nerve palsy, the lesion occurs in the cortex or between the cortex and the brainstem. The muscles of the ipsilateral eyelid and forehead are still supplied by intact nerve input from the contralateral side. On physical exam, this looks like drooping only of the contralateral side of the mouth. In peripheral facial nerve palsy, the lesion is distal to the brainstem or at the stylomastoid foramen. All the muscles of facial expression on the ipsilateral side will be paralyzed. On physical exam, this appears as drooping of the corner of the mouth, effacement of the nasolabial folds, inability to wrinkle forehead or raise the eyebrows, and incomplete closure of the eye. When asked to close eyelids, both eyes will roll superiorly (Bell’s phenomenon). https://www.aafp.org/afp/2007/1001/p997.html VIII. (Vestibulocochlear): Test hearing by finger rub on both sides. Ask patient to close their eyes while you hold your hand a few inches from their ears and rub your fingers together. Ask them to compare sides. (On a clinical exam, you won’t be asked to do the Rinne (pronounced Renée) or the Weber tests). IX.(Glossopharyngeal) and X (Vagus): Assess palatal elevation (“say ah”). Here, you’re looking for symmetric rise of the soft palate Note: CN IX and X are often considered together due to their close association anatomically when exiting the skull. They also frequently overlap and have similar peripheral patterns of distribution. When examining palatal elevation, look at the point where the uvula attaches to the soft palate. On a normal exam, the uvula should remain midline. If there is damage to the vagus nerve, the palate will elevate asymmetrically and the uvula will deviate away from the side of the lesion, as it is pulled toward the stronger constrictors on the intact side. as the patient says “ah.” Use your penlight to locate the soft palate and observe its rise XI. (Spinal Accessory): 1. Assess bilateral shoulder elevation (trapezius) muscle. Have patient shrug up both shoulders and hold them there against your downward resistance (“Don’t let me push you down”). 2. Assess strength of neck rotation (SCM). Have patient turn head to the right and then ask them to push their head back to center while you resist their attempt by placing your hand on the left side of their cheek/chin. Repeat with the opposite side. XII.(Hypoglossal): Assess midline tongue protrusion. Ask patient to stick tongue all the way out, then move tongue from side to side. Check for any atrophy and abnormal movements, such as fasciculations, which can be seen in denervating diseases, such as ALS. Note: Complete paralysis of CN XII results in hemiparalysis of the tongue. Resting in the mouth, the tongue curves to the healthy side, but on protrusion, it deviates to the affected side due to unopposed contraction of the intact genioglossus muscle1. E: Motor 1. Observe muscle bulk. Look for any asymmetry, atrophy, or weakness during the history- taking and while getting onto the exam table. Be aware of any abnormal or involuntary movements, such as jerking, fidgeting, or fasciculations. 2. Assess muscle strength. Move from top to bottom, proximal to distal. Test flexion and extension of each muscle group. It’s very important to test bilateral muscles simultaneously so you can compare both sides. Deltoids, Biceps, Triceps, Wrist Flexors and Extensors (make sure you support the forearm to isolate the wrist muscles), Lumbricals (patient spreads fingers wide and you try to push them together while they resist) Grip strength- cross your 2nd and 3rd fingers so you don’t get hurt. Try to pull your fingers out of their grip. Hip flexors (Iliopsoas), Knee flexors (Hamstrings), Knee extensors (Quadriceps), Ankle dorsiflexion (Tibialis Anterior), Plantar flexion (Gastrocnemius) Muscle Strength Rating scale (0-5/5) 0/5: No movement 1/5: Contraction visualized but no movement 2/5: Movement, but not against gravity, e.g. across surface 3/5: Movement against gravity but not resistance (e.g. they can lift up their arm but you can easily overcome the flexion or extension with no effort on your part) 4/5: You can overcome with some effort their flexion or extension 5/5: Normal. They can completely resist your attempts to overcome their flexion or extension Note: For ease of performance, develop a system with which to do your motor exam. It’s also helpful to not mix the motor exam with any other components of the neuro exam, such as the sensory component. Work superiorly to inferiorly, starting proximally and moving distally. 3. Assess pronator drift. Have patient hold out both arms at shoulder level, palms facing up, and close their eyes. Count to in your head to 3. A normal exam is when the patient’s arms stay in the original position and do not move. Pronator drift occurs due to a lesion in the corticospinal tracts which results in the weaker supinator muscles being overcome by the pronators and the weaker arm is unable to resist gravity. 4. Assess muscle tone. As you’re moving the patient around, assess muscle tone. How easily do the muscles move, how easily to the limbs flex and extend? Is there any rigidity (e.g. in Parkinsonism) or flaccidity (e.g. post-stroke)? You can test tone by rapidly flexing a patient’s arm a few times. Make sure the muscles are completely relaxed. A normal exam occurs when the arm flexes easily and smoothly. What’s the difference between spasticity and rigidity? Spasticity and rigidity both occur due to hypertonia. Distinguishing between the two is useful to localizing a lesion. Spasticity occurs due to damage to the corticospinal (pyramidal) tracts and is velocity and amplitude dependent. This means that rapidly flexing and extending the affected limb can elicit a sudden increase of tone or a “catch” of resistance to the movement. Moving the limb slowly doesn’t elicit the resistance4. Rigidity occurs due to dysfunction of the extrapyramidal tracts, particularly the basal ganglia or spinal cord. The increased muscle tone is constant and uniform in all directions of movement and is independent of velocity. The increased tone will be felt on examination with slow assisted flexion and extension of the affected limb. This is often described as “lead pipe” rigidity because moving the limb feels like attempting to bend a lead pipe4. Cogwheel rigidity occurs when there is a tremor overlying lead pipe rigidity4. F: Sensory Assess bilateral upper and lower extremities for sensation. Remember your neuroanatomy and recall that there are two ascending spinal tracts for sensation: spinothalamic and dorsal column-medial lemniscus (DC-ML) tracts. 1. Spinothalamic tract: pain and temperature 2. DC-ML: fine touch, vibration, two-point discrimination, proprioception Important note: For the exam, you’ll need to test both the spinothalamic and DC-ML tracts by testing only ONE function from each tract. You can pick which function you want to test. You DO NOT have to test ALL the sensations available for the CS exam but please practice all of them in Doctoring to get the proper technique. Thus, on the exam you only test, 1. Cold temperature (spinothalamic), OR pain via pinprick and, 2. Vibration OR position sense OR light touch (DC-ML) of the bilateral upper and lower extremities. To Test 1. Spinothalamic: Pain: Have patient close eyes. Open a clean safety pin and poke patient with the sharp end and the dull end alternately and randomly. Ask patient to tell you which end you’re poking them with, the sharp or the dull. Test all 4 extremities, proximal and distal. OR: take a long wooden Q- tip swab break off the end so you have a sharp woody end. Have patient close eyes and poke patient with either the sharp end or the soft cotton tip at random. Ask patient to tell you which end you’re using. Test all 4 extremities, proximal and distal. OR Temperature: Have patient close eyes as you touch all 4 extremities, proximal and distal, with the cold metal of your tuning fork or reflex hammer. Ask patient what temperature they feel. 2. DC-ML: Vibration: Hit a 128Hz tuning fork against the ball of your hand to make it vibrate. Have patient close eye as you hold vibrating tuning fork against all 4 extremities, proximal and distal (usually the tip of the finger and tip of the big toe), and ask patient to tell you when they feel the vibration stop. After a few seconds, stop the vibration with your hand. OR Position sense: Explain to patient that you’re going to move their thumb/toe up and down and you want them to tell you which way you’re moving it. Have patient close eyes and take their right hand in yours, grasp the digit by the lateral sides, and move it up and down at random. Repeat with the other thumb and both toes. Note: When testing position sense, it’s important to hold the digit by its lateral edges, as opposed to its top and bottom surfaces. Holding it from the top and bottom can falsely lead the patient to believe they know the position when they’re really feeling the top or bottom of their digit being pressed more firmly. OR Light touch: Have patient close eyes as you use your index fingers to lightly touch all 4 extremities, proximal and distal, and ask them if they can feel your touch. Touch bilateral upper and lower extremities simultaneously so patient can compare sides Note on neuroanatomy: Both ascending sensory pathways are contralateral. The spinothalamic tract originates with neurons in the dorsal root ganglion that extend axons into the dorsal horn and synapse with the second neuron of the pathway which crosses to the contralateral side in the spinal cord and has its cell body in the spinal cord gray matter and axon in the thalamus. In the DC-ML system the axon of the dorsal root ganglion neuron enters the dorsal root and dorsal column white matter in the spinal cord1,3. Axons of the dorsal column are arranged so that the fibers for the lower extremities are located medially (fasciculus gracilis) and the fibers for the upper extremities are located laterally (fasciculus cuneatus)3. Dorsal column axons then synapse with the second neuron in the medulla3. The second neuron then decussates in the medulla and ascends in the brainstem in the medial lemniscus bundle3. The axons terminate in the thalamus where they synapse with a third neuron, which projects to the postcentral gyrus of the cerebral cortex3. G. Reflexes Test the brachioradialis, biceps, triceps, patellar, ankle/Achilles and plantar/Babinski reflexes. Note: Adequate testing of the reflexes requires complete relaxation of the muscles, which may be difficult for the nervous or ticklish patient. If a patient is tense, try having them squeeze their fists together while testing the lower extremity reflexes, or kick their legs out in front of them and hold them up while you’re testing the upper extremities. Using your finger to palpate the tendon is especially useful here. Your finger provides a little extra stretch on the tendon and prevents you from repeatedly hitting blindly at the patient with your reflex hammer. To test the Babinski reflex: scrape the sharp end of your reflex hammer (or your thumbnail) upwards along the lateral edge of the sole of the foot in a firm, sweeping motion and across the ball of the foot. Doing this can elicit a variety of responses, from a normal quick upwards jerk of the foot and quick curling of the toes, to a pathologic slow withdrawal and flexion of the ankle, knee, and hip (triple flexion), to the Babinski sign. Babinski sign: Slow and deliberate dorsiflexion of the big toe and fanning out/abduction of the other toes. Indicates damage to upper motor neurons in the corticospinal tract. Grading the reflexes (0-4/4) 0/4: no movement 1/4: Hypoactive, slow to react, minimal motion 2/4: Normal 3/4: Hyperactive, brisk reflexes, exaggerated movement. May have intermittent clonus 4/4: Hyperactive with Sustained clonus Clonus: A series of slow, rhythmic, involuntary muscle contraction. H. The Cerebellum/Coordination 1. Finger to nose. “Using your right index finger, touch my finger, then touch your nose as fast as you can.” Hold your finger far enough so the patient’s arm is completely extended reaching for it. Move your target finger around so they at least have to reach left, right, up, and straight. Repeat on the opposite side. Movement should be smooth and quick. Note: Look for dysmetria, which is a sign of lateral lobe cerebellar dysfunction. Dysmetria is defined as a horizontal, back and forth motion of the limb as the patient attempts to touch the target, over-/undershoots, and tries to correct themselves. This sequence of motions looks jerky and fragmented and not smooth as it would normally be1. Dysmetria can be confused with motor weakness. Weakness, however, manifests as a vertical, up and down fragmentation of movement as the patient tries to overcome gravity to meet the target. 2. Heel to shin. Ask patient to run right heel continuously up and down the front of the left shin as fast as they can. Repeat on the opposite side. Normally, this motion should be smooth and unbroken and the heel should stay in contact with the shin. I: Gait and Balance 1. Gait Walk across the room as patient normally would. Note any abnormal movements, placement of the feet (e.g. wide-based gait), shuffling of the gait, and placement and motion of the arms. Ask patient to turn around and walk back. Observe how patient turns, if they turn in one smooth motion, or if it takes them several small steps to turn around. a. Walk across the room on the tips of their toes. Walk away from examiner to better assess subtle abnormalities such as foot drop. b. Walk across room on heels only. Walk on heels when returning to the examiner. c. Tandem walk: have patient walk heel-to-toe, as if they’re on a tightrope. 2. Romberg’s sign. Have patient stand in the room with their feet together and arms at their sides and close their eyes. Count in your head to 3. A normal test occurs when a patient can maintain their balance with their eyes closed. Tests proprioceptive input and the midline vermis function of the cerebellum. Sources 1. Ropper AH, Samuels MA, Klein JP. Adams and Victor’s Principles of Neurology, 10 th Ed. New York: McGraw Hill, 2014. 2. NIH Stroke Scale, http://www.nihstrokescale.org 3. http://library.open.oregonstate.edu/aandp/chapter/14-5-sensory-and-motor-pathways/ 4. https://www.movementdisorders.org/MDS/Journals/Clinical-Practice-E- Journal- Overview/Clinical-Practice---Volume-2-Issue-2/How-Do-I-Examine- Rigidity-and- Spasticity.htm ** By: Christine Meadows, MSIV ** Contributions by: Dr. Paul Turner, Dr. Amy Robinson, Lauren Hatcher, MSIV, and Judea Wiggins, MSIV Version 1/25/2019 Updated: Diana Greene-Chandos MD, FNCS on 8/15/20 High Yield Notes- LUMBAR SPINE EXAMINATION: Low Back or Spinal Radiculopathy Examination Components 1. Inspect the Lower Back. View from the side noting the lumbar concavity and whether it is flattened or exaggerated. View from behind noting and skin irregularities or masses as well as the alignment of the iliac crests. 2. Palpate the spine. With the patient sitting or standing palpate the bony prominences of the lumbar spine with your thumb. Start at the level of the umbilicus and first palpate midline looking for increased pain or any palpable deformities (aka “step offs” for subluxation). Then move to palpate laterally each segment into the sacral spine and then out to palpate the sacroiliac joint (pain here can be seen in sacroiliitis and/or Ankylosing Spondylitis). In addition to palpation- perform gentle percussion along the spinal process and see if this elicits any pain which can be seen in osteoporosis, infection (spinal abscess) or malignancy. 3. Palpate the paraspinous musculature Looking for tenderness and spasm. Muscles in spasm feel firm and knotted and may be visible. 4. Perform low back ROM testing (see normal ROM degrees below) a. Have patient flex forward as far as they can- “touch your toes!” b. Have patient extend spine back- it helps sometimes if the patient puts their hands on their hips to do this “Bend as far back as possible” c. Have patient laterally bend to the right and then to the left- “Bend to the side from the waist” Examiner can assist by placing hand on the patient’s hip if needed- please do this from the front and explain/ask permission from patient to place your hand on their hip d. Have patient rotate the spine “Rotate from side to side”. 5. Straight Leg Raise for Radiculopathy Diagram below shows the technique for radiculopathy specifically demonstrating L5 nerve root- but also works for S1. Have the patient lay flat on their back with legs straight out and slowly lift the leg. Patient may feel pulling or tension in their low back or hamstrings, but we are specifically looking for nerve pain- shooting, burning, stabbing, or tingling going down the leg. Note: to test for L4 radiculopathy (not pictured in the diagram- symptoms typically are pain shooting into the quadriceps area to the knee)- have patient lie on their stomach with legs straight. Then moving the leg by holding the ankle flex the leg slowly at the knee, bringing the foot to the gluteal area. This test would be positive if nerve pain occurred in the quadriceps to knee area. HIGH YIELD NOTES- Taking a Neurological History I. Headache History a. Onset- Hyper-acute (“thunderclap”= subarachnoid hemorrhage); Acute- Cluster Headache and Migraine Headache; Sub-acute- Tension Headaches, Cervicogenic Headaches/Occipital Neuralgia, Meningitis, sinus headache; Chronic- Tumor-related headache; medication-overuse headache; TMJ b. Location Plus: Subarachnoid Hemorrhage- initially may be whole head and then settles to the back of the head and down the neck; Meningitis- Back of the head mainly but can involve the whole head; Tumor-related headache- behind eyes and whole head; Medication overuse- tension like but can involve whole-head. c. Quality Migraine Headache- throbbing/pounding/pulsating Tension Headache- squeezing Cervicogenic Headache with Occipital Neuralgia- Muscle ache/stiffness/soreness (neck component) and Shooting/burning pain up the back of the head (occipital neuralgia component TMJ- soreness/achy pain in masseter and jaw Sinus Headache- pressure sensation +/- throbbing in face Medication over-use- can be either like tension or like migraines typically Cluster Headache- a deep extremely severe pounding/punch/stab sensation Subarachnoid Hemorrhage- sudden severe overall explosive/pounding/pressure pain Meningitis- throbbing pain (back of the head) with stiffness of neck Tumor Headache- pressure/fullness d. Quantity- varies, SAH and cluster are often described as 10/10; Migraine headaches at their worst tend to be 5-10/10- all others can be highly variable. e. Aggravating Items: Migraine- light (photophobia) and sound (phonophobia); certain foods like chocolate, coffee, or red wine Tension- sleep deprivation; continued tension/stress; teeth clenching/grinding Cervicogenic HA/ Occipital neuralgia- poor posture (“tech neck”), pressure on back of the head TMJ- grinding/clenching teeth, chewing Sinus Headaches- bending forward Medication Over-Use- missing acetaminophen or ibuprofen or any other repeatedly used medication Cluster Headache- UNKNOWN Meningitis- Flexing the neck and straight leg raise while lying flat Tumor Headache- lying flat f. Alleviating Items: Migraine- rest, acute migraine medications Tension- rest, massage Cervicogenic HA/Occipital neuralgia- massage, physical therapy, injection of xylocaine or lidocaine at the greater occipital protuberance TMJ- jaw relaxation techniques, muscle relaxing medications, dental prosthetics, anti- inflammatories Sinus Headaches- anti-histamines, decongestant medications, sinus saline washes, steam, OTC pain medications Medication Over-Use- taking the medication that was “missed” Cluster Headache- Oxygen, Triptan medications Meningitis- relaxing neck, anti-inflammatories Tumor Headaches- sitting or standing (head upright) g. Associated Symptoms: Migraine- nausea, vomiting, visual changes (aura), +/- numbness or weakness Tension- can trigger a secondary migraine headache Cervicogenic HA/Occipital Neuralgia- numbness in the back of the head or pain radiating into the shoulder or arm TMJ- jaw clicking noise, molar shape changes due to grinding Sinus Headaches- rhinorrhea, fever Medication Over-Use- can trigger a secondary migraine headache Cluster Headache- rhinorrhea, tearing, conjunctival redness, ptosis Meningitis- fever, chills, nausea, may have a variety of neurological symptoms and seizures Tumor Headaches- nausea, vomiting, may have a variety of neurological symptoms depending on location II. Ischemic Stroke History- Major Questions a. Time of onset? If not known, then last time known to be normal. b. Symptoms? Weakness/ Numbness/ Slurred Speech (Dysarthria)/ Difficulties Understanding Language/ Difficulties finding words or unable to speak at all/ Dizziness/ Loss of Vision/ Double Vision (diplopia)/ Facial Droop/ Difficulties Walking or Balance Difficulties c. Symptoms that come and go, are steady, have improved or are getting worse d. Prior history of stroke/TIA e. What were you doing at the onset of stroke? f. Any Headache? g. History of Hypertension? (a risk for stroke) h. History of High Cholesterol? (a risk for stroke) i. History of Diabetes? (a risk for stroke) j. History of Coronary Artery Disease (CAD)? (if there is CAD, there is a high likelihood of cerebrovascular disease) k. History of Atrial Fibrillation or frequent “racing” heart or skipped beat symptoms? l. History of Carotid Artery Disease? (if there is significant carotid disease there is a high risk of stroke) III. Seizures- Major Questions a. Description of Seizure? (ie loss of consciousness? Memory of event? What did bystanders describe: shaking all over after falling down or slumping over; stopping and staring with blinking or smacking lips) b. Any warning of oncoming seizure (called a seizure aura) like smell of burning or metal; dizziness; epigastric rising (sensation when elevator rises too fast) c. Post-seizure feeling- fatigue, body aches or normal d. Any tongue biting or trauma? e. Any urinary incontinence? f. Are seizures new or prior history? g. How often are seizures? h. Any triggers for seizures (ie lack of sleep, missing medications, drinking alcohol) i. Any seizure medications regularly? j. Underlying reason for seizures (prior head trauma, prior meningitis/encephalitis) IV. Multiple Sclerosis- Major Questions a. New Diagnosis- describe deficits (numbness, weakness, vision loss, dizziness, double vision, loss of balance, facial pain or numbness) b. Prior issues? Specifically ask about being diagnosed with optic neuritis (loss of vision) in the past c. Prior MRIs of the brain or spine? d. Where did you grow up (looking for northern climates)? e. Any memory issues? f. If already diagnosed with MS- when was last episode/exacerbation; last MRI; what MS medications are you taking? V. Low Back Pain- Major Questions a. Onset- Acute: Muscular source, Radiculopathy (disc herniation); Chronic: Arthritic (Spinal Stenosis), Muscular Source and Radiculopathy (disc herniation) b. Location: Muscular source- typically paraspinal muscle (erector spinae) and upper gluteal areas; Bony Source (midline spine or sacroiliac joints); Disc herniation with radiculopathy (depends on the disc level)- pain down the back or front of leg c. Quality- Muscular source- sore, dull, achy, feels like a muscle pull; Bony Source- sore, dull, intermittent throbbing, pain with deep palpation; Disc/Radicular Source- sharp, burning pain down the leg or into the hip d. Quantity- Highly variable can be minor or 10/10 for all sources of back pain e. Aggravating Items: Muscular source- bending forward or to the side, lifting, twisting; Bony Source- back extension, pressure on midline back or iliosacral spine, sitting; Disc/Radicular Source- sudden movements, lying flat, sitting, sneezing, twisting spine, bending forward or backwards, straight leg raise f. Allieviating Items: Muscular Source- heat, stretching, massage, physical therapy, muscle relaxing medications; Bony source- physical therapy, gentle traction, ibuprofen; Disc/radiculopathy Source: Physical therapy, gentle traction, ibuprofen, gabapentin g. Associated Symptoms: Muscular Source- hip pain, middle and upper back pain; Bony Source: multiple areas of joint pains; sacroiliac pain- can be associated with iritis, uveitis (in ankylosis spondylitis); Disc/radicular Source- numbness, weakness in the nerve affected; Bowel and bladder dysfunction (cauda equina syndrome); Sneezing Low Back Pain with Radiculopathy from Hooten, WM and Cohen, SP “Evaluation and Treatment of Low Back Pain: A clinically focused review for primary care physicians” Mayo Clinic Proceedings- Symposium on Pain Medicine: 90 (12) pp 1699-1718; December 2015 Low back pain (LBP) is a leading cause of disability worldwide with a lifetime incidence of 51% to 84%.Classification of LBP based on the distribution of pain as predominately axial (pain localized to the low back area) or radicular (pain radiating to the lower extremities in a dermatomal distribution with or without accompanying LBP) is particularly relevant to primary care specialists because the distribution of pain is often a corollary of frequently occurring disease processes involving the lumbar spine. The estimated prevalence of LBP varies according to the surveillance period and specific type of pain. For example, in a systematic review, the point prevalence of LBP was 18.3%, the 1-month rate was 30.8%, and the mean annual prevalence was 38.0%. In a more recent systematic review in which chronic LBP was defined as pain lasting longer than 12 weeks, the prevalence ranged from 5.9% to 18.1%. The 1-year incidence of an initial episode of LBP ranges from 6.3% to 26.2% and estimates of recurrence at 1 year range from 24% to 80%. Neuropathic pain, defined as pain resulting from a lesion or disease affecting the somatosensory system, can be an important characteristic of LBP especially in individuals with a herniated disc causing nerve root irritation and lumbar spinal stenosis. In individuals with predominately chronic axial LBP, questionnaires designed to detect the distinguishing characteristics of neuropathic pain have found that between 17% and 55% of individuals have pain that is primarily neuropathic in nature, with a median rate of 41%. This distinction is important because neuropathic pain may be associated with greater levels of physical and psychological dysfunction as compared with other types of pain. The incidence of new-onset radicular pain ranges from 1.5% to 18.5%, and the incidence of lumbar spinal stenosis has been estimated to be 5 per 100,000 people. Although the anatomy of the lumbar spine is complex, several key anatomical structures contribute to commonly encountered clinical problems including the vertebral body, intervertebral disc, facet joint, paraspinal muscles, and ligamentum flavum. The lumbar spine is composed of 5 vertebrae. The intervertebral disc is an avascular fibrocartilaginous structure that allows movement between adjacent vertebral bodies (Figure 1). Each lumbar intervertebral disc is approximately 4 cm in diameter and 7 to 10 mm in thickness, and it is composed of an outer annulus fibrosus and an inner nucleus pulposus. The annulus is a dense concentric ring of layered collagen fibers that surrounds the nucleus and resists tensile forces. The nucleus pulposus contains collagen and elastin fibers embedded within a hydrated proteoglycan gel. Disc degeneration is associated with annular tears and dehydration of the nucleus pulposus, which can lead to decreased disc height, impaired mechanical function, rupture, and compression of spinal nerve roots (Figure 2). In addition, nerve and vascular ingrowth into the disc and exposure of these nerves to inflammatory mediators have been associated with axial LBP. Lumbar facet joints, also referred to as the zygapophysial joints, are true synovial joints formed by the superior and inferior articulating processes of 2 adjacent vertebrae. The inferior aspect of each lumbar facet joint is innervated by the medial branch of the posterior primary rami at the same level of the facet joint, and the superior aspect is innervated by the medial branch from 1 level above. This dual innervation is important when considering targeted diagnostic and interventional therapies for lumbar facet pain. From a biomechanical perspective, the 2 facet joints and the intervertebral disc at each spinal level are interdependent and form what is referred to as a motion segment, otherwise termed the three-joint complex. In this manner, the lumbar spine can be conceptualized as a stacked series of motion segments. Whereas the intervertebral disc is the principal weight- or load-bearing structure of each motion segment, the role of the facet joints is to limit torsion and resist forward displacement of the vertebral segment. However, in the setting of degenerative disc disease and associated disc space narrowing, the total load transmitted to the facet joint increases and can sometimes exceed 50% of the total load placed on the vertebral segment. , Pathophysiologically, osteoarthritic changes involving the lumbar facet joints are common and include joint space narrowing due to degenerative thinning of the cartilage, presence of inflammatory cells and mediators, increased vascularization, subchondral bone remodeling, and osteophyte formation, which can contribute to axial LBP and spinal stenosis. These osteoarthritic changes, particularly osteophyte formation, can contribute to neural foraminal stenosis and compression of the exiting nerve root, which can lead to the development of radicular pain. The ligamentum flavum extends along the posterior aspect of the vertebral column and connects the laminae of the adjacent vertebrae. The ligamentum flavum is 2- to 3-mm thick and is composed of elastin and collagen fibers in a 2:1 ratio; the elastin fibers provide elasticity, and the collagen fibers provide tensile strength and stability. Hypertrophy of the ligamentum flavum is multifactorial and has been associated with older age, mechanical stress, increased body mass index (calculated as the weight in kilograms divided by the height in meters squared), and alterations in cytokine and proteinase inhibitor concentrations. Ligamentum flavum hypertrophy can be an important contributor to the development of spinal stenosis, especially when it occurs in conjunction with other disease processes that narrow the spinal canal, including facet joint arthropathy and disc protrusions. Multiple muscles affect lumbar spine function and can be categorized into 3 major anatomical groups relative to the torso: the posterior, anterior, and lateral groups. Together, these 3 muscle groups control movement of the spine, contribute to the stabilization of the vertebral column, and provide proprioceptive feedback. The posterior group, composed of superficial (ie, erector spinae and serratus posterior inferior), intermediate (ie, longissimus thoracis), and deep (ie, multifidus and quadratus lumborum) layers, arise from the transverse and spinous processes of the vertebrae and insert on the iliac crests and sacrum. The deeper muscles span fewer vertebrae compared with the more superficial muscles, and the muscles more adjacent to midline are of greater diameter. The muscles of the posterior group are responsible for extending, lateral bending, and torsion of the spine. The anterior group is chiefly composed of the abdominal wall (ie, rectus abdominis, external oblique, and internal oblique) and is primarily responsible for flexion of the spine, but these muscles also contribute to lateral bending and torsional movement. The lateral group includes the psoas and iliacus muscles. The psoas muscle arises from the lateral aspects of the lumbar vertebrae, and the iliacus muscles arise from the anterior ilium and lateral sacrum. These 2 muscles join as they move laterally to insert on the lesser trochanter of the femur and are often referred to as the iliopsoas muscle. The iliopsoas is a powerful flexor of the thigh and works to maintain an upright and erect posture. Current evidence suggests that the cross-sectional area and density of paraspinal muscles are reduced in patients with LBP, and alterations in muscle activation and fat infiltration of the paraspinal muscles have been observed in these patients. In addition, reduced paraspinal muscle density has been associated with facet joint osteoarthritis, spondylolisthesis, and disc space narrowing. The differential diagnosis of axial LBP is broad but commonly involves lumbar spine structures that include the intervertebral discs, facet joints, sacroiliac joints, and paraspinal musculature. Although nonspecific, some historical features and characteristic signs and symptoms associated with axial LBP may be helpful in determining the source of pain. The intervertebral disc can be a source of pain in up to 40% of patients with axial LBP. These patients tend to be younger (age 65 years). Lumbar facet pain is generally worsened by prolonged standing and relieved with sitting or recumbency, which decreases the load on the joints. In some patients, pain may be localized to the paraspinal region with or without radiation to the groin, thigh, or occasionally distal to the knee. On physical examination, no test is considered to be sensitive for identifying a painful facet joint. Although small and methodologically flawed studies suggested that pain with extension and axial rotation was indicative of facet arthropathy, diagnostic studies using double local anesthetic and placebo-controlled facet blocks, cadaveric studies using infrared markers, and correlative studies evaluating lumbar facet radiofrequency denervation outcomes have all refuted this assertion. , Sacroiliac joint pain occurs in 15% and 30% of individuals with axial LBP and is associated with a specific inciting event in 40% and 50% of occurrences; motor vehicle collisions and falls are 2 of the most common causes. Patients will often report pain in the gluteal or paraspinal (below the fifth lumbar vertebra) regions with or without radiation to the thigh, but up to 28% of patients may have referral of pain distal to the knee. Although discogenic pain is often characterized by sitting intolerance, sacroiliac joint pain may be worsened during transitional movements, such as rising from a sitting position. On physical examination, previous studies suggest that a combination of physical maneuvers rather than a single test can accurately identify patients with sacroiliac joint pain. In the differential diagnosis of sacroiliac joint pain, it is important to rule out piriformis muscle syndrome. The piriformis muscle originates from the inner surface of the sacrum and attaches to the greater trochanter of the femur. Unilateral or bilateral buttock pain with radiation in an L5 or S1 dermatomal distribution (when impingement on the sciatic nerve is present) is characteristic, and pain intensity typically fluctuates throughout the day. On physical examination, transgluteal buttock tenderness can often be elicited, pain can sometimes be provoked by maneuvers that stretch the muscle (eg, adduction and internal rotation of the hip), and the straight leg raising test result is typically negative, which help distinguish piriformis muscle syndrome from radicular pain. Axial LBP related to the paraspinal muscle or ligament strain is often precipitated by both strenuous and nonstrenuous activities including heavy lifting, repetitive movements, spinal torsion, or trauma. The onset of pain is generally delayed by 1 to 2 days and is often localized to the lumbosacral region. On physical examination, hypomobility due to muscle spasm or guarding may be evident, and pain may be reproduced with palpation of the paraspinal musculature. Although any muscle or ligament can potentially be affected, frequently involved structures include the multifidus, quadratus lumborum, erector spinae, and psoas muscles, as well as interspinous and supraspinous ligaments. Myofascial pain may be an important contributing factor to other sources of LBP or a primary cause by itself and is characterized by the presence of trigger points that are hyperirritable tense bands of skeletal muscles. Patients will typically present with a history of localized or regional pain, and the range of motion may be reduced in the affected muscles. On physical examination, palpation of a trigger point will typically provoke sharp localized pain that may be referred to a contiguous body region, although this can be difficult, if not impossible to discern, in nonsuperficial muscles. Herniated Intervertebral Disc Similar to axial LBP, the differential diagnosis of radicular pain is broad, but approximately 90% of cases in the nonelderly are caused by a herniated intervertebral disc at the L4-L5 or L5-S1 level. Another important source of radicular pain includes foraminal stenosis, which is common because of far lateral disc herniation or facet joint hypertrophy. An inciting event may or may not be identified, but some patients report experiencing a “pop” in the region of the lumbar spine followed by the gradual onset of pain over the next 1 to 2 days. However, the single most important historical factor is the distribution of pain, which should follow a dermatomal pattern, though approximately one- third of people have multiple affected dermatomes. In contrast to nociceptive pain, neuropathic LBP is often described as a sharp, lancinating, or burning sensation. Patients may report that pain is worsened by forward bending, coughing, sneezing, or prolonged sitting and improved with recumbency. When localizing the affected nerve root on the basis of the dermatomal distribution of pain, it is important to recognize that each nerve root exits the spinal column beneath the pedicle of the vertebral body with the same number as the nerve. For instance, the L4 nerve root exits beneath the pedicle of the L4 vertebral body, which is situated above the interspinal disc at this level. Therefore, disruption of the disc situated between the L4 and L5 vertebrae will typically impinge the traversing L5 nerve root (unless it is a far lateral herniation that accounts for 50 MME/day is considered a high dose, and should be carefully titrated >90 MME/day is exceptionally high; documentation regarding the reason for this dose is very important People who non-pharmacologic and non-opioid therapy are not effective for People with severe, acute pain Who Should Opioids be Prescribed To? Discussions to have prior to prescribing opioids 1 2 3 Establish realistic Discuss risks and Explain the role of goals with patient benefits with Naloxone and its including pain level patient importance and functional changes Checklist before Prescribing Opioids Check Check the state Prescription Drug Monitoring Program (PDMP) Obtain Obtain urine drug screen Depending on institutional guidelines, draft and explain the ”Pain Contract” with Discuss patient Screen Screen patients’ other medications for potential interactions This is a document drafted by the provider or institution It is a contract signed by the provider and patient that states: The provider should be the only person from whom the patient receives opioids, and the patient should What is a only use one pharmacy Explains the risks and benefits of the medication, as ”pain well as the importance of Naloxone availability The patient and provider agree to certain boundaries contract”? to be kept, and certain checkpoints (patient will complete a urine drug screen every 6 months, and prescriptions will be monitored from the PDMP) These can be complex documents; feel free to ask your preceptor about their experience with them! Guidelines for Opioid Prescriptions Prescribe immediate release rather than extended release Start at the lowest effective dose For acute pain, prescribe for the shortest duration of pain likely (3 days is a good baseline) If more medication is needed, patients should meet with their provider to discuss their pain and have an assessment References https://www.cdc.gov/mmwr/volumes/65/rr/rr6501e1.htm?CDC_AA_ refVal=https%3A%2F%2Fwww.cdc.gov%2Fmmwr%2Fvolumes%2F65% 2Frr%2Frr6501e1er.htm#B1_down https://www.cdc.gov/drugoverdose/pdf/calculating_total_daily_dose -a.pdf https://journalofethics.ama-assn.org/article/what-does-good- pharmacist-physician-pain-management-collaboration-look/2020-08 https://www.cdc.gov/opioids/data/analysis- resources.html#anchor_trends_in_deaths_rates Multiple Sclerosis- Clinical Script Multiple sclerosis (MS) is a chronic autoimmune, inflammatory neurological disease of the central nervous system (CNS). MS attacks the myelinated axons in the CNS, destroying the myelin and the axons to varying degrees. The course of MS is highly varied and unpredictable. In most patients, the disease is characterized initially by episodes of reversible neurological deficits, which is often followed by progressive neurological deterioration over time. From 250,000 to 350,000 patients in the U.S. have MS, and 50% of patients will need help walking within 15 years after the onset of the disease. Twice as many women are affected as men, and persons of Northern European descent appear to be at highest risk for MS. The disease is diagnosed on the basis of clinical findings and supporting evidence from ancillary tests, such as magnetic resonance imaging (MRI) of the brain and examination of the cerebrospinal fluid (CSF). MS typically presents in adults 20 to 45 years of age; occasionally, it presents in childhood or late middle age. The cause is unknown, but it appears to involve a combination of genetic susceptibility and a nongenetic trigger, such as a virus, metabolism, or environmental factors, that together result in a self-sustaining autoimmune disorder that leads to recurrent immune attacks on the CNS. Neurologists agree that patients may be grouped into four major categories based on the course of disease: 1. Relapsing–remitting MS: the most common form, affecting about 85% of MS patients. It is marked by flare-ups (relapses or exacerbations) of symptoms followed by periods of remission, when symptoms improve or disappear. 2. Secondary progressive MS: may develop in some patients with relapsing–remitting disease. For many patients, treatment with disease-modifying agents helps delay such progression. The disease course continues to worsen with or without periods of remission or leveling off of symptom severity (plateaus). 3. Primary progressive MS: affects approximately 10% of MS patients. Symptoms continue to worsen gradually from the beginning. There are no relapses or remissions, but there may be occasional plateaus. This form of MS is more resistant to the drugs typically used to treat the disease. 4. Progressive-relapsing MS: a rare form, affecting fewer than 5% of patients. It is progressive from the start, with intermittent flare-ups of worsening symptoms along the way. There are no periods of remission. There is no single diagnostic test for MS. The diagnosis is based on evidence of (1) at least two different lesions (plaques or scars) in the white matter of the CNS (the space dissemination criterion); (2) at least two different episodes in the disease course (the time dissemination criterion); and (3) chronic inflammation of the CNS, as determined by analysis of the CSF (the inflammatory criterion). The presence of one or more of these criteria allows a general diagnosis of MS, which may be refined according to the subsequent course of the disease. An international panel on the diagnosis of MS suggested that the time dissemination criterion should be confirmed by clinical signs on MRI at least 3 months after the previous clinical episode or on a previous MRI. The panel also suggested that the inflammatory criterion could replace the space dissemination criterion when the latter is missing at the clinical and paraclinical levels. To make a diagnosis of MS, the physician must: At autopsy, multiple, discrete pink or gray areas that have a hard, rubbery texture are identified within the white matter. The lesions are composed of areas of myelin and oligodendrocyte loss along with infiltrates of inflammatory cells, including lymphocytes and macrophages. The relative preservation of axons and neurons within these lesions helps to differentiate MS from other destructive pathological processes that are accompanied by focal inflammation. More than 30% of MS patients have moderate-to-severe spasticity, mostly in the legs. Initial clinical findings in MS patients are often sensory disturbances, the most common of which are paresthesias (numbness and tingling), dysesthesias (burning and “pins and needles”), diplopia, ataxia, vertigo, and bladder (urinary sphincter) disturbances. A common manifestation of MS is unilateral numbness affecting one leg that spreads to involve the other leg and rises to the pelvis, abdomen, or thorax. Sensory disturbances usually resolve but sometimes evolve into chronic neuropathic pain. Trigeminal neuralgia also occurs. Another common presenting sign of MS is optic neuritis, highlighted by complete or partial loss of vision. Bladder dysfunction occurs in more than 90% of MS patients and results in weekly or more frequent episodes of incontinence in one-third of patients. At least 30% of patients experience constipation. Fatigue occurs in 90% of patients and is the most common work-related disability associated with MS. Sexual problems are often experienced as well. The goals of therapy with disease-modifying agents in patients with MS include shortening the duration of acute exacerbations, decreasing their frequency, and providing symptomatic relief. No curative, FDA-approved therapies for MS are currently available. Symptomatic treatments are aimed at maintaining function and improving quality of life. It is common practice to treat acute relapses of MS with a short course (typically 3 to 5 days) of a corticosteroid that has a rapid onset of action and that produces few adverse drug effects (AEs), such as intravenous (IV) methylprednisolone or dexamethasone. Brief courses of corticosteroids (e.g., oral prednisone 60 to 100 mg once daily, tapered over a period of 2 to 3 weeks, or IV methylprednisolone 500 to 1,000 mg once daily for 3 to 5 days) are also used to treat acute exacerbations and to shorten the duration of MS attacks. Although there is no cure for MS, FDA-approved therapeutic agents can reduce disease activity and progression in patients with different types of MS. From: Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria, Thompson, Alan J et al. The Lancet Neurology, Volume 17, Issue 2, 162 - 173 Six out of the 12 cranial nerves play crucial roles in the functioning of the vision, the eye and its surrounding structures. Similar to other parts of the nervous system these nerves can be categorized into afferent and efferent pathways. The afferent pathway is primarily associated with the optic nerve (CNII), responsible for transmitting visual information. Meanwhile, the efferent pathways involve CNIII, IV, and VI, which control eye movements, and for CN III also the upper eyelid elevation. Sensation in the eye is mediated by the trigeminal nerve (CNV), while the CNVII is responsible for facial motor functions, including those related to the eye. Additionally, the sympathetic nervous system plays a role in lifting the eyelids and dilating the pupil. The coordinated activity of these neural pathways ensures the optimal functioning of the visual system. Focusing on CNII, commonly referred to as the optic nerve, serves a crucial function in vision. Its primary role is to transmit visual information from the retina of each eye to the brain, specifically the visual cortex in the occipital lobe. It can be damaged due to intracranial hypertension, variety of metabolic disorders, vascular diseases, intracranial masses and diseases such as multiple sclerosis (MS). Evaluation of the optic nerve typically involves assessing visual acuity, visual field testing, and a thorough examination of the optic disc, which is the point where the optic nerve enters the eye. See below for details. A comprehensive eye examination is a critical skill for all providers as it allows for thorough assessment of ocular complaints and timely intervention. Many eye conditions can be asymptomatic while causing serious permanent damage. Obtaining a detailed medical history and conducting a basic eye examination can help identify warning signs of blinding eye diseases (such as glaucoma, diabetic retinopathy, and macular degeneration), systemic diseases (like diabetes and hypertension), and brain- related disorders (including tumors, aneurysms, and multiple sclerosis). Detecting these issues early can facilitate prompt treatment or referral to an ophthalmologist, potentially preserving both vision and overall health. From a neurology standpoint, these skills are critically important because it allows for proper workup, improved diagnostics, and early detection of catastrophic disease. Fundus Anatomy (Figure 1): Retina: sensory portion of the eye, Peripheral Retina contains layers of photoreceptors, Peripheral Retina nerve fibers. Macula/Fovea: pigmented area of the retina responsible for central vision. Optic Rim Optic Cup The fovea is a small pit within the Macula macula involved in the extreme Optic Nerve (CNII) central vision. Optic Nerve ▪ Optic Disk: entry and exit point of Optic Disk Fovea the eye; vessels and nerve fibers come together here to form the optic nerve. ▪ Optic Cup: physiologic indentation Peripheral Retina Retinal Vessels Peripheral Retina within the disk that is normally less than 1/3 the disk diameter. Figure 1: Fundus Anatomy (see below for bigger & unlabeled images). Important in assessing the health of the nerve. ▪ Neural Rim: space between the inner cup and surrounding disk. Blood Vessels (arteries vs. veins): provides to and drain blood from retina. The vessels entering the eye are the central retinal artery and the central retinal veins. As a reminder, these are branches of the ophthalmic artery which supply the arteries and the veins that drain to the central retinal vein. Summary Steps in a Basic Eye Exam 1. Full HPI, including PMH, FHx, Allergies and medications 2. Measure the visual acuity (best correct vision) for each eye [CN II] 3. Perform a confrontational field test (peripheral vision) for each eye [CN II] 4. Test pupillary response, both direct and indirect [CN II and sympathetics] 5. Inspect the eyelids and surrounding tissues [CN III, V and VII] 6. Test extraocular movements [CN III, CN IV and CN VI] 7. Inspect conjunctiva and sclera 8. Use direct ophthalmoscope to study the fundus (back of the eye) including the disk, vessels, and macula. [optic nerve (CN II), Retina and optic vessels] Using the Direct Ophthalmoscope (Figure 2): A Step-by-Step Guide (for more details, please referred to Direct Ophthalmoscopy Video on Brightspace) 1. Preparation: Have the patient comfortably seated with the lights dimmed (promote dilatation) and looking at distance (avoids accommodation). Viewing Window 2. Set the diopter dial (focusing power) to +10 (green) and the aperture to the medium, round, white light. Filter 3. Using the same eye as the one you are examining, Switch Aperture begin 1 foot away and look through the viewing Dial window; assess for the red reflex. Note: place your free hand on patient shoulder for orientation. Diopter Dial 4. Slowly come close to the patient at a 15 angle Diopter Dial temporally while keeping the pupil in view. Turn the diopter dial in the negative direction (brings the retina into focus) 5. When the vessels come into view, follow them to the Brow Rest optic nerve. Viewing Note: the branches form an arrow pointing towards the nerve. Window 6. Examine the fundus: a. Optic nerve noting the color, cup-to-disk (C/D) ratio and the disk sharpness. b. Retinal Circulation noting AV nicking, emboli, Diopter and/or infarcts. Power Display c. Macula/Fovea noting color, cherry red spot, scar tissue or neovascularization. On/Off d. Peripheral Retina noting for any detachments, Switch cotton-wool spots, Roth spots, infarcts, or hemorrhages. Figure 2 Ophthalmoscope Parts: Patient side (top) and 7. Repeat for the second eye. Practitioner side (bottom). Note: make sure to also switch scope to your other eye. Important points: The view through the direct ophthalmoscope is limited (Figure 3); To examine all important structures the provider must look around the entire fundus. Figure 3 View with direct ophthalmoscope; undilated view (left), dilated view (right) Common Diseases based on Exam Findings: Red reflex abnormalities (Figure 4): Absent: ▪ Cataracts: Lens opacities blocking passage of light. ▪ Vitreous hemorrhage: Blood in the vitreous humor. ▪ Retinal detachment: detached retina away from normal position. Abnormal: ▪ Retinoblastoma: rare retinal neoplasia affecting young children. A B Figure 4 Red Reflex: normal reflex (top), absent reflex left eye (middle), abnormal reflex (bottom). Optic nerve cupping (Figure 5B):

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