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Neurology Disorders of MovementUMN vs LMNUMN vs LMN Upper Motor Neuron Lower Motor Neuron Paralysis Tone Reflexes Atrophy OtherUMN vs LMN Upper Motor Neuron Lower Motor Neuron Paralysis Spastic Flaccid Tone Hypertonic Hypotonic Reflexes Hyperreflexia Hyporeflexia Atrophy Disuse Wasting Other Babinski Sign + Babinski Sign - No Fasciculations Fasciculations Present Pronator Drift Ankle ClonusPronator DriftCase 1 One year ago, the patient, a 24-year old male, noticed • Mild muscle atrophy in hands and lower general weakness and cramping in his legs while extremities including the quadriceps and calf playing football, which led to numerous falls on the muscles field over several games. He spoke with his family doctor after two weeks of frequent falling and • Visible fasciculations of quadriceps bilaterally cramping. His family doctor referred him to a • Reduced strength throughout all four limbs neurologist. • Increased tone throughout limbs • + Babinski’s Sign • + Ankle Clonus • HyperreflexiaMotor Neuron Disease Clinical Features • Combination of UMN and LMN Signs • Eye Movement usually spared • Sensation Preserved • FasciculationsCase 2 Patient was admitted to the hospital presenting withExam concussion and whiplash injury due to an MVA. He is day 18 post-accident (day 13 post-hospital-discharge).tient has a wide base of support and presents with He is able to shower and dress independently but hasreduced gait speed and short stride length. Also, the some trouble with fine motor tasks such as buttoningpatient has increased upper body/trunk movement up his shirt or zipping up his trousers. during gait. Patient presents with slow eye movements and with some compensatory head turning movement. Nystagmus noted. No changes in sensation, reflexes normal. Babinski and clonus negative.Cerebellar Syndromes Dysdiadochokinesis Ataxia Nystagmus Intention Tremor Slurred Speech HypotoniaCase 3 History This 5 y.o. boy had a neck abscess three weeks ago. That was treated with drainage and antibiotics. Now, he presents with lower extremity weakness. Exam • Absent deep tendon reflexes both lower extremities • Diminished reflexes both arms • Spinal Tap CSF: Showed elevated protein levels of a week later admission and 132 mg/dl on follow-upGullian-Barre Syndrome Ascending Symmetrical Weakness Loss of Reflexes +/- Peripheral Sensation LossMiller Fisher Syndrome Ascending Descending Symmetrical Weakness Loss of Reflexes +/- Peripheral Sensation Loss + OpthalmoplegiaCase 4 59 y.o. man three months ago acute onset of Examination neurologic symptoms. He has developed generalized Orientated to person, place and time. hypokinesia, masked facies, tremors, and dysmetria. Able to recall 3 items immediately but diminished Additionally, his short term memory function has become severely compromised. He also reports recall after 20 minutes (1/3 items) rapidly progressive ataxia, speech abnormalities, Only able to follow 2-step commands diplopia. He has lived in Germany for 20 years as Language fluent but phrase length diminished enlisted spouse. No prior history of neurologic disease No pronator drift or early dementia in her family. He has three adult Hyperreflexia noted children who are all healthy and living in the states.Case 4Creutzfeldt -Jakob disease Defining Symptoms Dementia + Myoclonus Common Symptoms Ataxia Behavioral Changes HyperekplexiaCase 5 A 74 year old man experiencing difficulties with regular tasks around the house because he was experiencing ‘shaking’ and noticed a lot of his movements were much slower and difficult to ‘get going’. His son suggested he see his doctor after witnessing him have difficulty entering the front door of his home, ‘he was frozen and needed guidance to step in’. Prior to these symptoms, the patient recalls losing his sense of smell intermittently and noticed his handwriting becoming smaller but dismissed these as part of “getting old”.Case 5 A 74 year old man experiencing difficulties with regular tasks around the house because he was Resting tremor "pill-rolling". Cogwheel experiencing ‘shaking’ and noticed a lot of his rigidity pronounced in the upper extremities and mild-moderate rigidity in the trunk and movements were much slower and difficult to ‘get lower extremities. Bradykinetic movement, going’. His son suggested he see his doctor after dysmetria, and mild-moderate difficulty with witnessing him have difficulty entering the front door rapid alternating movement. of his home, ‘he was frozen and needed guidance to step in’. Prior to these symptoms, the patient recalls losing his sense of smell intermittently and noticed his handwriting becoming smaller but dismissed these as part of “getting old”.Parkinson’s Disease Typical Parkinson’s Triad Tremor Rigidity BradykinesiaParkinson’s Disease Symmetrical vs Asymmetrical Tremor Idiopathic = Asymmetrical Drug-Induced = SymmetricalParkinson’s Disease vs Lewy Body Dementia Parkinson’s Disease Motor Symptoms followed by Dementia symptoms over a year after onset Lewy Body Disease Motor symptoms arise concurrently or within a year of Dementia symptomsParkinson’s Disease st Treatment 1 Line: Levodopa (if motor symptoms affect life) 2 Line: Rasagiline (MAO-B inhibitor), Ropinirole (Dopamine Agonist)Multiple Sclerosis Clinical Features • Spastic Weakness • Optic Neuritis • Lethargy Charcot’s Neurological Triad • Dysarthria • Nystagmus • Intention TremorMultiple Sclerosis Pathophysiology • Demyelination of the CNS • Formation of plaques on different nerve pathways lead to neurological deficitsMultiple SclerosisMultiple Sclerosis Treatment Acute Relapse: Methylprednisolone Relapsing Remitting: Immunomodulators (Eg. INF-Beta)Charcot-Marie-Tooth DiseaseCharcot-Marie-Tooth Disease Clinical Features Foot Drop High Arch Feet Hammer Toes ‘Champagne Bottle’ Legs Cold Peripheries WeaknessSubacute Combined Degeneration of the Cord Caused by Vitamin B12 Deficiency Vitamin B12 MUST be given first when treating combined B12 and Folate deficiencySubacute Combined Degeneration of the Cord Clinical Signs • Proprioception + Vibration Sense Lost UMN Symptoms: • Weakness • Hyperreflexia • Babinski’s + Typical Triad: • Babinski’s + • Brisk Knee Jerks • Absent Ankle JerksCase 6 A 28-year-old man presented to the emergency department for low back pain and numbness in both lower extremities. Two days earlier, he had sharp, shooting pains in the back and buttocks after moving boxes. The pain was relieved with hydrocodone with acetaminophen. However, on the morning of presentation, the patient awoke with numbness in both lower extremities and had left leg weakness so severe that the patient was unable to stand or walk without support. The patient described the pain as mild while he was supine and worse when he sat or stood. The patient reported some urinary hesitancy, dribbling of urine, and constipation. He did have morning erections. The patient reported that he had had an industrial injury five years before that resulted in a herniated lumbar disk and subsequent laminectomy; he had been doing well since then until the time of presentation.Cauda Equina Clinical Features • Lower Limb Weakness • Sacral Numbness • Areflexia • Urinary RetentionCauda Equina Investigations • PR Examination • MRI Sacral SpineCauda Equina Treatment • Urgent Surgical DecompressionCase 7 History 82 year old woman presents with symmetrical, progressive leg weakness with a tingling sensation on the extremities for the past 3 years. She also reports that she now needs to rest on the way to the shops due to feeling that she ”cannot get enough air in.” However in regards to her muscular fitness, she mentioned that when she first had the weakness, she would just need to ”walk it off” before she could get the strength back. She reports no past cardiac or respiratory medical history and reports she is typically fit and well, but has lost some weight due to her reduced appetite.Case 7Lambert-Eaton vs Myasthenia Gravis Lambert-Eaton Myasthenia Gravis Autonomic Dysfunction Present Absent Reflexes Decreased Present Exercise Strength Improves Strength Worsens Tumour Small Cell Lung Cancer Thymus Eye Involvement Symmetrical Weakness Other Ascending Weakness Asymmetrical Weakness Descending WeaknessLambert-Eaton vs Myasthenia Gravis Lambert-Eaton Myasthenia Gravis Antibodies against Voltage Gated Antibodies against Acetylcholine Calcium Channels Receptors on NMJ PathophysiologyLambert-Eaton vs Myasthenia Gravis Lambert-Eaton Myasthenia Gravis Treatment of Small Cell Lung Cancer Pyridostigmine +/- (Acetylcholinesterase Inhibitors) Amifampridine Treatment