PaEasy Neuro Test bank question and answers, graded A+. 2022

PaEasy Neuro Test bank question and answers, graded A+. 2022 Document Content and Description Below PaEasy Neuro Test bank question and answers, graded A+. 2022 A 75-year-old man is involved in a motor vehicle accident and strikes his forehead on the windshield. He complains of neck pain and severe burning in his shoulders and arms. His physical examination reveals weakness of his upper extremities. What type of spinal cord injury does this patient have? A anterior cord syndrome B central cord syndrome C Brown-Séquard syndrome D complete cord transection E cauda equina syndrome - Central Cord Syndrome the central cord syndrome involves loss of motor function that is more severe in the upper extremities than in the lower extremities, and is more severe in the hands. There is typically hyperesthesia over the shoulders and arms. Anterior cord syndrome presents with paraplegia or quadriplegia, loss of lateral spinothalamic function with preservation of posterior column function. Brown-Séquard syndrome consists of weakness and loss of posterior column function on one side of the body distal to the lesion with contralateral loss of lateral spinothalamic function one to two levels below the lesion. Complete cord transection would affect motor and sensory function distal to the lesion. Cauda equina syndrome typically presents as low back pain with radiculopathy. A 17-year-old boy develops progressively abnormal muscle fatigability. He is diagnosed as suffering from myasthenia gravis and is admitted into a hospital. In the course of his treatment with pyridostigmine, he develops increased weakness, nausea, vomiting, sweating, and bradycardia. What is the best management for this patient? Answer Choices 1 Thymectomy 2 Corticosteroids 3 Plasmapheresis 4 Withdrawal of pyridostigmine 5 Addition of neostigmine - Withdrawal of pyridostigmine Explanation The patient is having a cholinergic crisis. The over-dosage of cholinesterase inhibitors, such as pyridostigmine and neostigmine, results in cholinergic crisis; it is characterized by salivation, lacrimation, urinary incontinence, emesis, and other symptoms like colic, diarrhea, and miosis. These symptoms are similar to myasthenic crisis, and because treatment differs in both, the 2 conditions need to be differentiated. After stabilizing the patient, edrophonium testing should be done in order to distinguish between a myasthenic and a cholinergic crisis. The management of patients with cholinergic crisis involves prompt withdrawal of cholinesterase inhibitors. The immediate administration of atropine is also recommended. Thymectomy is indicated in severe cases of myasthenia gravis. It is especially effective in young women. Steroids sometimes help if immunosuppression is needed for thymoma, which may be associated with myasthenia gravis. Plasmapheresis is a treatment for severe cases of myasthenia gravis with or without thymectomy. Neostigmine is an alternative cholinesterase inhibitor. There is no rationale in switching from pyridostigmine if a cholinergic crisis has already occurred. A 33-year-old African-American woman presents with a new onset of left facial droop. The droop was present when she awoke this morning, and it has worsened since then. She reports that she had been feeling fine. She denies headaches, visual changes, and weakness or tingling in the extremities. Exam reveals an anxious, overweight woman. She is afebrile. Cranial nerve exam reveals weakness of the entire left side of the face, including the forehead. The left eye does not close entirely, and there is a widened palpebral fissure. Sensation is intact. All cranial nerves, other than VII, appear intact. Her tympanic membranes are clear, and there are no skin lesions around the face or head. The rest of her exam is unremarkable. Labs reveal normal CBC, serum electrolytes, thyroid function tests, and liver transaminases. A chest X-ray is clear. Question What is the most likely cause of this patient's facial droop? Answer Choices 1 Bell's palsy 2 Sarcoidosis 3 Ramsay-Hunt syndrome 4 Lyme disease 5 Cerebrovascular accident (CVA) - Bell's Palsy Explanation This patient has a classic presentation of Bell's palsy. Bell's palsy is a sudden, unilateral facial weakness and affects about 1 out of every 60 or 70 persons in their lifetime. The etiology is unknown at this time, but herpes simplex virus type 1 has been associated with some cases. The presumed pathogenesis of the palsy is that inflammation of the facial nerve causes swelling then secondary compression, and ischemia occurs where the nerve courses through the temporal bone. Pain behind the ear may precede the paralysis by a day or 2. Hyperacusis and loss of taste may occur, if the lesion is proximal enough; lacrimation may be affected as well. Sensation is not affected, although patients may experience numbness or heaviness in the face. In some cases, there is a mild lymphocytosis of the CSF. MRI may reveal swelling and uniform enhancement of the geniculate ganglion and facial nerve. Also, in some cases, MRI may reveal a swollen facial nerve entrapped within the temporal bone. Prognosis depends upon the degree of paralysis. Approximately 80% of patients will recover within a few weeks to a month. Of those with an incomplete paralysis in the 1st week, nearly all will experience complete recovery within several months. Of those with a more complete paralysis, like this patient, nerve conduction studies and electromyography can indicate prognosis. The likelihood of completely recovery is 90% if the nerve branches in the face retain normal excitability to supramaximal electrical stimulation; however, the likelihood is only about 20% if electrical excitability is absent. Treatment includes symptomatic care, such as taping the upper eyelid closed during sleep and using lubricating agents in the eye In order to prevent corneal desiccation. Some studies have shown improvement in patients treated with glucocorticoids; other studies showed improvement with prednisone and acyclovir together. Sarcoidosis can cause a form of bilateral facial paralysis (facial diplegia) called uveoparotid fever (Heerfordt's syndrome). Given this patient's African American background, sarcoidosis should be considered as a possible etiology of her symptoms. However, the unilateral nature of the paralysis, combined with a negative chest X-ray, makes sarcoidosis unlikely. A serum angiotensin converting enzyme (ACE) could be drawn if sarcoidosis is a concern. Ramsay-Hunt syndrome is a facial palsy associated with a vesicular eruption in the pharynx, external auditory canal, and other surrounding areas of skin. This is thought to be secondary to herpes zoster infection of the geniculate ganglion; often the 8th cranial nerve is affected, as well. This patient did not have any skin lesions around the ear, thus making this diagnosis very unlikely. However, this demonstrates the importance of a thorough examination in facial palsy patients, including careful examination inside the ears. Lyme disease is a frequent cause of facial paralysis in areas where Lyme infection is endemic. However, the majority of patients who have facial palsy caused by Lyme disease note an antecedent rash adjacent to the site of a tick bite. Blood tests for Lyme disease can help identify that as an etiology. However, this patient denied any risk factors for tick bites such as camping/ travel, making this diagnosis less likely. The family history of CVA and the fact that she is currently taking oral contraceptives do confer some increased risk for thrombotic events in this patient. However, with a stroke, the forehead is usually spared from facial palsy, since the upper facial muscles (the frontalis and orbicularis oculi muscles) are innervated by corticobulbar pathways from both motor cortices. The lower facial muscles are innervated only by the contra-lateral hemisphere. This patient's facial palsy is complete and includes the forehead because the facial nerve itself is affected in Bell's palsy. A 13-year-old boy presents with dysmorphic features (e.g., a long face, prominent jaw, and large ears), large testes, and intellectual disability (intellectual developmental disorder). History reveals that 2 other family members also have intellectual disability. Question What is the most likely clinical diagnosis in this child? Answer Choices 1 Klinefelter syndrome 2 Noonan syndrome 3 Patau syndrome 4 Fragile X syndrome 5 Prader-Willi syndrome - Explanation The most likely clinical diagnosis is fragile X syndrome; it accounts for 3% of cases of intellectual disability (intellectual developmental disorder). Macroorchidism and hereditary intellectual disability are 2 specific features of this syndrome. Fragile sites are regions of chromosomes that have a tendency for separation, breakage, or attenuation under particular growth conditions. 1 fragile site associated with fragile X syndrome is on the distal long arm of chromosome Xq27.3. In Klinefelter syndrome, most children (80%) have a male karyotype with an extra X,47,XXY. The remaining 20% have a higher grade of sex chromosome aneuploidy, (i.e., 48,XXXY; 49XXXXY; 48,XXYY). Klinefelter syndrome is the most common cause of hypogonadism and infertility in boys/men; puberty occurs at the normal time, but the testes and penis remain small. Noonan syndrome is an autosomal dominant disorder. Clinical features are similar to Turner syndrome, but Noonan syndrome affects both sexes, while Turner syndrome occurs only in girls/women. Clinical features include a short stature, a low posterior hairline, a shield-like chest, and a short webbed neck. Pulmonary stenosis due to valve dysplasia is the most common cardiac anomaly in Noonan syndrome. In Turner syndrome, the common cardiac defects are bicuspid aortic valve, coarctation of aorta, aortic stenosis, and mitral valve prolapse. Patau syndrome (trisomy 13) is characterized by intellectual disability (intellectual developmental disorder), cleft lip and palate, microcephaly, low-set ears, central nervous system malformations (e.g., holoprosencephaly), and microphthalmia. Prader-Willi syndrome manifests with hypotonia, intellectual disability (intellectual developmental disorder), hypogonadism, and hyperphagia (leading to obesity). Some children with Prader-Willi syndrome have a partial deletion of the paternally derived chromosome 15 and loss of paternally-expressed genes. A 54-year-old man presents after having a generalized seizure. The patient is HIV positive, but he has been unable to afford antiretroviral therapy since losing his job 2 years ago. Other than cachexia, the physical exam is unremarkable. Upon further inquiry, the patient also notes that he has become short-tempered and hypercritical; at times he seems confused. An MRI of the brain is performed, and it reveals several cortical ring-enhancing lesions. Question What is the most likely diagnosis? Answer Choices 1 AIDS dementia complex 2 Cryptococcal meningitis 3 Cytomegalovirus encephalitis 4 Progressive multifocal leukoencephalopathy 5 Toxoplasma encephalitis - Toxoplasma encephalitis Explanation The patient's symptoms and MRI findings are most consistent with the diagnosis of toxoplasma encephalitis. Toxoplasmosis is the most common cerebral mass lesion among HIV-positive patients. Infection with the Toxoplasma gondii parasite is relatively common and usually asymptomatic. Reactivation occurs in HIV-positive patients due to failing cellular immunity, and it causes a multifocal necrotizing encephalitis. Seizures may be the initial manifestation of central nervous system (CNS) infection; other common clinical manifestations include focal neurologic deficits (e.g., impaired speech and hemiparesis). Personality change, lethargy, headache, and confusion are also observed. The MRI in patients with toxoplasma encephalitis characteristically reveals multiple, ring-enhancing lesions with surrounding edema; these lesions usually occur bilaterally in the frontal and parietal cortices. AIDS dementia complex describes a constellation of cognitive symptoms seen among HIV-positive patients. The condition occurs when the HIV virus disseminates to the CNS. Within the CNS, the virus tends to concentrate in the basal ganglia and subcortical regions. Symptoms include a constellation of cognitive, behavioral, and motor disturbances that cause varying degrees of functional impairment. Characteristic MRI findings include non-enhancing white matter, cerebral atrophy, and ventricular enlargement. The diagnosis requires that other central nervous system infections, carcinoma, general medical conditions, and substance abuse have been excluded. Cryptococcal meningitis is caused by the encapsulated fungus Cryptococcus neoformans. Among HIV-positive patients, the illness may be the result of new infection or reactivation of latent infection. Presenting signs are often nonspecific; they include headache, fever, change in mental status, and nausea or vomiting. Nuchal rigidity and photophobia may also be present, and elevated intracranial pressure is not uncommon. MRI findings vary, but they include lesions in the basal ganglia; meningeal enhancement, cerebral edema, and shrunken ventricles may also be seen. Cytomegalovirus (CMV) infection causing encephalitis is usually observed in patients with evidence of CMV infection at other sites. MRI findings vary, but they often show areas of focal necrosis within the brain parenchyma, meninges, or periventricular regions. Symptoms typically reflect progressive dementia, with episodes of confusion, apathy, and focal neurologic deficits. Progressive multifocal leukoencephalopathy is often a fatal disorder; it is caused by reactivation of a latent JC viral infection. Focal neurologic deficits (e.g., hemiparesis and gait disturbance) are often the initial presenting symptoms; they are followed by progressive cognitive decline, coma, and death. The MRI commonly reveals multiple, non-contrast enhancing foci in the cerebral white matter. A 48-year-old Caucasian woman with a past medical history of hypertension and hypercholesterolemia was diagnosed recently with a cerebral aneurysm. The treatment plan for the aneurysm is endovascular coiling. Among other complications, this patient has an increased risk of thromboembolism postoperatively. Question What is the initial preventive medication that will be used to help minimize this risk in this patient? Answer Choices 1 Abciximab 2 Heparin 3 Coumadin 4 Eptifibatide 5 Tirofiban - Heparin Explanation Complications of endovascular coiling can include thromboembolism and intra-procedural aneurysm rupture. A study found the incidence of thromboembolism in up to 12.5 % of patients in their patient population group. For this reason, many providers will choose to administer some type of combination of heparin and/or antiplatelet therapy to help minimize this potential complication. Coumadin is not indicated as an appropriate choice for this acute procedure. The medications abciximab, eptifibatide, and tirofiban are all anti-platelet/glycoprotein IIb/IIIa inhibitors. These all have been shown to be safe, but they are currently only recommended for use in percutaneous coronary intervention and the prevention of complications in patients with unstable angina/non-ST-elevation myocardial infarction. A 70-year-old woman is brought to your attention by her family because of the slowly progressive gait disorder, the impairment of mental function, and urinary incontinence. About 1 year ago, she started having weakness and tiredness in her legs, followed by unsteadiness; her steps became shorter and shorter, and she also experienced unexplained backward falls. She is becoming emotionally indifferent, inattentive, and her actions and thinking have became "dull". Over the past month, she has started having urinary urgency and involuntary leaking of urine. Besides multivitamins and local application of the Timolol for glaucoma, she takes no other medications; there are no other symptoms. Question What is most likely the best method of treating the patient's urinary problems? Answer Choices 1 Antimuscarinic drug (Tolterodine) 2 Antibiotic (Sulfamethoxazole/trimethoprim) 3 Acetylcholinesterase inhibitor (Donepezil) 4 Ventriculoperitoneal shunt 5 Kegel exercises - Ventriculoperitoneal shunt Explanation Clinical triad of slowly progressive gait disorder, followed by impairment of mental function and then sphincteric incontinence strongly suggests the presence of normal-pressure hydrocephalus. Ventricular expansion is the cause of symptoms, and surgical CSF shunting is the main treatment modality. The potential benefit from surgery is usually evaluated by testing gait, cognition, and micturition before and after CSF drainage. Antimuscarinic Tolterodine is an antispasmodic that is used for symptomatic treatment of urinary incontinence in patients with an overactive bladder (urge incontinence). Antimuscarinic drugs are contraindicated in patients with glaucoma. A urinary tract infection will probably manifest with a strong, persistent urge to urinate, burning sensation when urinating, passing frequent, small amounts of urine that has unusual smell and the appearance. Your patient has no such signs and symptoms; therefore, in this case, antibiotics are not indicated. Donepezil is used to treat dementia, but in the case of normal-pressure hydrocephalus, the problem is anatomic (the distortion of the periventricular limbic system and frontal lobes), and the best treatment is probably surgical. Kegel exercises can prevent or control urinary incontinence and other pelvic floor problems in cases of pelvic sphincter weakness. However, pelvic sphincter weakness will probably manifest as stress incontinence. What is the treatment of choice for primary generalized seizures? Answer Choices 1 Phenytoin 2 Phenobarbital 3 Valproic acid 4 Carbamazepine 5 Gabapentin - Valproic acid Explanation