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Kingdom of Bahrain Arabian Gulf University College of Medicine and Medical Sciences. Neurology and ICU (Review) Year 5 – Internal Medicine. Presented by: Dr. Taysir Prepared by: Ali Jassim Alhashli. Neurology – Cranial Nerves.
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Kingdom of BahrainArabian Gulf UniversityCollege of Medicine and Medical Sciences Neurology and ICU (Review) Year 5 – Internal Medicine Presented by: Dr. Taysir Prepared by: Ali JassimAlhashli
Neurology – Cranial Nerves • Comparison between Upper Motor Neuron Lesion (UMNL) and Lower Motor Neuron Lesion (LMNL): • Lesion of an upper motor neuron might be in the cortex or in the pyramidal tract and extending until anterior horn cells of the spinal cord. • Lesion of a lower motor neuron might be in the muscle itself or in in neuromuscular junction or in the nerve or anterior horn cells of the spinal cord.
Neurology – Cranial Nerves • CN-VII (facial nerve) paralysis: • Muscles which are controlled by facial nerve include: frontalis, orbicularisoculi, orbicularisori, baccinator and nasalis. • How to test? • Ask the patient to rise his eyebrows (and check for wrinkles of forehead), close his eyes against resistance applied by the examiner, smile (angle of the mouth will be deviated towards the normal side of the face but there will be drooling of saliva at the affected side), blow cheeks against resistance applied by the examiner. • Upper motor neuron lesion: affecting lower half of the face at the opposite side of the lesion. • Lower motor neuron lesion: affecting half of the face at the same side of the lesion (Bell’s palsy).
Neurology – Cranial Nerves • CN-III (oculomotor nerve): • If there is a defect, what would be the manifestations? • Ptosis. • Squint (if the defect is in the right CN-III → the right medial rectus muscle will be paralyzed → therefore, patient will not be able to look to the left side with his right eye). • Dilation of pupils. • Notice that the cavernous sinus which is draining blood from the brain has the passage of these three cranial nerves: • CN-III (oculomotor nerve). • CN-IV (trochlear nerve). • CN-VI (abducens nerve). Any increase in pressure in this sinus will can affect these nerves.
Neurology – Diseases • Stroke: • It can be: • Hemorrhagic: appearing as a white lesion with CT-scan of the head. • Ischemic: appearing as a dark lesion with CT-scan of the head. • What are the causes of ischemic stroke? • Source of emboli from the heart (especially if patient has atrial fibrillation, arrhythmias, endocarditis, ASD or left ventricle thrombus). • Carotid artery stenosis. • Thrombus in situ: which means that a thrombus might develop in cerebral arteries themselves. • Prognosis: unpredictable and depends on re-circulation in the brain after the stroke. • Management of patient with stroke: • Heparin is contraindicated in hemorrhagic infarction. • Antiplatelets (aspirin). • Anti-coagulants are given when there is a permanent source of emboli.
Neurology – Diseases • Myesthenia gravis: • What is it? • Generalized fatigue, inability to elevate eyelids for a long time (patient has bilateral partial ptosis). Notice that respiratory arrest might occur if diaphragm is affected. • Diagnosis: • Check for the presence of acetylcholine receptor antibodies. • Administer edrophonium and watch for patients symptoms getting better. • EMG: decreased muscle contractions with repetitive nerve stimulation. • Treatment: • Anti-cholinergics: such as neostigmine. • Thymectomy: effective in many patients. • IVIG and plasmapheresis: lowering the level of circulating antibodies. • Prognosis: poor with no cure for the disease.
Neurology – Diseases • Parkinson’s disease: • Site of the lesion: basal ganglia and specifically in dopaminergic neurons of substantianigra (which is present in the floor of the brain). • Etiology: • Idiopathic. • Trauma. • Drug-induced (anti-psychotics, methyldopa, metoclopramide and reserpine). • Infectious processes (such as meningitis and encephalitis). • Clinical manifestations: • Hypokinesia. • Rigidity (cog-wheel). • No habituation with glabellar reflex (myerson’s sign). • Positive jaw reflex. • Central gravity in patients with Parkinson’s disease is shifted anteriorly with short-steppage gait. • Management: • Pharmacological: levodopa + carbidopa (most common). • Surgical: deep brain stimulation of subthalamic nuclei.
ICU – Shock • Hypovolemic shock: • Example: patient presenting with vomiting, diarrhea and he is severely dehydrated (with presence of signs of dehydration). In addition, patient is stuperous. • In hypovolemic shock, you will find the following: • Right-atrial pressure: very low (because there is no venous return). • Cardiac output: very low. • Systemic vascular resistance: increased. • Cardiogenic shock: • Notice that it has all risk factors and features of an acute myocardial infarction. • In cardiogenic shock, you will find the following: • Right atrial pressure: increased. • Occlusion pressure of pulmonary artery: increased. • Cardiac output: decreased. • Systemic vascular resistance: increased.
ICU – Shock • Septic shock: • Example: patient presenting with high-grade fever, a source of septecemia, un-recordable blood pressure. In addition, he is stuperous and warm (keep in your mind that peripheries are usually cold in shock). • In septic shock, you will find the following: • Right atrial pressure: normal. • Occlusion pressure of pulmonary artery: normal. • Cardiac output: increased. • Systemic vascular resistance: very low due to intense vasodilation resulting in the undetectable blood pressure.
ICU – Fluid and Electrolytes • Hyperkalemia: • Notice that acute hyperkalemia can be caused by the following: • Acute renal failure. • Adisson’s disease. • Drugs: such as spironolactone and amalioride. • Crush syndrome: huge amount of skeletal muscle necrosis. • Clinical manifestations: you must worry about arrhythmias mainly. ECG shows peaked T-wave and prolonged PR-segment. • Management: • Calcium gluconate. • Insulin/glucose infusion in a 1:3 ratio given over 2 hours. • Calcium resonium (mainly rectal).
ICU – Fluid and Electrolytes • Hyponatremia: • Definition: Na > 110 mmol/L. • Clinical manifestations: convulsions, lethargy, patient becomes stuperous and might end with coma or death. • Rapid replacement of sodium can result in pontinemyelinolysis which is irreversible if it occurs. • Management: • Replacement by: 10-12 mmol/day. • Correction is done using half strength normal saline. • Dilutionalhyponatremia: due to fluid excess. Although it is not true but patient will be symptomatic. This condition is managed with restriction of water intake.
