History

Fact Explanation
Introduction to the disease It is a rare form of posterior circulation stroke of the brain. A lesion within the tegmentum of the midbrain can produce Benedikt Syndrome.[1]. Disease is characterized by ipsilateral third nerve palsy with contralateral hemitremor.[2].
Diplopia Diplopia or the double vision resulted due to ipsilateral oculomotor nerve palsy resulted due to involvement of oculomotor nucleus.[1].
Contralateral hemiparesis Damage to the other structurs such as corticospinal tract resulted in contralateral hemiparesis. It is a distinct finding in Benedikt's syndrome.[1].
Tremor Fascicular injury in the area of the red nucleus can leads to oculomotor nerve palsy with contralateral hemitremor due to damage to cerebral afferents to the thalamus.[2]. Some studies suggest that mechanism of tremor in Benedikt's syndrome is associated with the cerebellofugal pathway and the rubrospinal tract. [3].Different names including rubral tremor, midbrain tremor, thalamic tremor etc are used to describe this tremor.[4].
Ataxia Superior cerebellar peduncle and/or red nucleus damage in Benedikt Syndrome can further lead in to contralateral cerebellar hemiataxia.[1].
History of smoking Smoking is a known risk factor for stroke.Smoking can increases the risk of stroke by about 6 folds.[5].
History of hypertention Hypertension is identified risk factor for development of stroke. About 90% of strokes occur in patients with resistant hypertension ,among patients who receiving treatment for hypertension,HT has a contribution for atherosclerosis. But HT itself causes small vessel disease lead in to stroke.[5]
History of diabetes Diabetes also a known risk factor for development of stroke.[6].
History of hypercholesterolemia Hypercholesterolemia increase the risk of atherosclerosis thereby increase risk of stroke.[5],[6].
Family history of stroke Having positive family history of stroke increase the risk of individual to get a stroke.[6].
References
  1. RUCHALSKI K, HATHOUT GM. A Medley of Midbrain Maladies: A Brief Review of Midbrain Anatomy and Syndromology for Radiologists Radiol Res Pract [online] 2012:258524 [viewed 06 October 2014] Available from: doi:10.1155/2012/258524
  2. KHAN ARIFO. Pupil-sparing complete third nerve palsy from cryptogenic midbrain stroke in an otherwise-healthy young adult with patent foramen ovale. Middle East Afr J Ophthalmol [online] 2012 December [viewed 06 October 2014] Available from: doi:10.4103/0974-9233.95260
  3. FUJIEDA T, YAMAUCHI T, TAKAHASHI S, MOROJI T. Letter: Effect of levodopa on tremor in Benedikt's syndrome. Br Med J [online] 1974 Mar 9, 1(5905):456-457 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1633264
  4. ALUSI S. H.. Stereotactic lesional surgery for the treatment of tremor in multiple sclerosis: A prospective case-controlled study. [online] 2001 August, 124(8):1576-1589 [viewed 06 October 2014] Available from: doi:10.1093/brain/124.8.1576
  5. SPENCE J. DAVID. Intensive risk factor control in stroke prevention. F1000Prime Rep [online] 2013 October [viewed 06 October 2014] Available from: doi:10.12703/P5-42
  6. NICOL MB, THRIFT AG. Knowledge of Risk Factors and Warning Signs of Stroke Vasc Health Risk Manag [online] 2005 Jun, 1(2):137-147 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1993942

Examination

Fact Explanation
Ptosis Ptosis or drooping of eye lid also a manifestation of 3rd nerve palsy. 3rd nerve palsy causes paralysis of the levator palpebrae muscle that results in ptosis.[1].
Deviation of the eye Eye is deviated to Downward and outward.Occurs due to ipsilateral third nerve palsy. Injury to the oculomotor nerve causing damage to the extraocular muscles results in downward and lateral deviation of the eye.[1].
Dilated unresponsive pupils Examination of pupils will show dilated unresponsive pupils. These afferent pupillary defect is a manifestation of 3rd nerve palsy.[1].
Contralateral hemiparesis Damage to the corticospinal tracts will result contralateral hemiparesis.[1].
Motor incoordination Involvement of the superior cerebellar peduncle and/or red nucleus cause motor incoordination.[1].
Ataxia Gait assessment during examination reveals cerebellar contralateral ataxia. Occurs due to an insult to the structures such as red nucleus and fibers of the superior cerebellar peduncle.[1]
Higher function assessment findings. It includes memory, orientation, language and attention.Cognitive deficits appear in approximately 30% of stroke patients. However it is found to be unimpaired in most patients with Benedikt syndrome.[2],[1]
References
  1. RUCHALSKI K, HATHOUT GM. A Medley of Midbrain Maladies: A Brief Review of Midbrain Anatomy and Syndromology for Radiologists Radiol Res Pract [online] 2012:258524 [viewed 06 October 2014] Available from: doi:10.1155/2012/258524
  2. HEBB ANDREA L. O., BRANDMAN DAVID, SHANKAR JAI, HEBB ADAM O.. Visualizing Recovery of Cognitive Function in Stroke. JBBS [online] 2013 December, 03(08):641-652 [viewed 06 October 2014] Available from: doi:10.4236/jbbs.2013.38067

Differential Diagnoses

Fact Explanation
Intra cranial hemorrhage (ICH) Sudden onset focal neurological deficit that progresses over minutes to hours is the classic presentation of ICH. It is accompanied by headache, nausea, vomiting, elevated blood pressure and decreased consciousness. The symptoms are related to the site of hemorrhage. Ataxia initially found in cerebellar hemorrhage, and weakness may be the initial symptom in patients with basal ganglia hemorrhage. Compared to ischemic stroke, headache and vomiting are more common in patients with ICH at the onset of disease.[1]
Posterior circulation ischemic stroke It is the infarction occurring within the vascular territory supplied by the vertebrobasilar arterial system.They present with sudden and maximal at onset stroke symptoms. The common presenting symptoms include vertigo, imbalance, slurred speech, double vision,unilateral limb weakness, headache, nausea, and vomiting. Unilateral limb weakness, gait ataxia, limb ataxia, nystagmus and dysarthria are the examination findings. Dysphagia due to pharyngeal weakness, nausea, vomiting, and Horner’s syndrome may resulted in the proximal PC territory Infarcts. Weakness and nuclear facial palsy resulted in infarction in middle territory where as decreased appendicular sensory loss, lethargy, visual field defects are found in infarction in distal territory.[2].
Primary brain tumors Primary brain tumors are rare. About 30% tumors are benign and the malignant tumors are fatal most of the time. Most patients develop headache. Epilepsy is another feature. Other features include hemiplegia, motor weakness, confusion, dysphasia, memory loss, and personality change. Visual disorders and papilloedema also can be recognized.[3].
Tuberculous meningitis The duration of symptoms prior to presentation can be be vary from 1 day to 6 month. Fluctuation of non specific features such as fatigue, malaise, anorexia, vomiting, fever, and headache can be seen during this period. Some patients may present with progressive dementia, associated with social withdrawal as well as personality changes.Cranial nerve palsies can be seen on presentation, most commonly with the involvement of 6th nerve. Second, third, fourth, eighth nerves also can get involved.Seizures may occur in some individuals. Pyramidal or cerebellar signs may resulted due to cerebral edema or brainstem infractions.Deep coma, spasticity and posturing may seen in end stage of the disease.[4].
Hemiplegic migraine It can be sporadic or familial. Motor aura of hemiplegic migraine is unique feature. Usually there is no jerking before the onset of weakness.The weakness is found to be twice as likely to affect the arm as the leg. It can be last for hours to days. The hemiplegia is almost always accompanied by head pain.[5].
Cavernous sinus thrombosis It causes manifestation of 3rd nerve palsy. However there are several other nerves can get involved. It causes paralysis of multiple cranial nerves, including the trigeminal (V1 and V2), trochlear (CN IV), and abducens (CN VI) nerves. [6].
Transient ischemic attacks (TIA) A transient episode of neurological dysfunction caused by a focal brain, spinal cord, or retinal ischaemia, without acute infarction is called as TIA. However maximum duration of 24 h can be variable. They may present with hemiparesis in both anterior and posterior circulation TIAs. Carotid territory ischaemia causes aphasia and transient monocular visual loss. Vertebrobasilar ischaemia causes bilateral limb weakness, vertigo, hearing loss, either haemianopia or diplopia. Abrupt onset of maximal symptoms predicts a final diagnosis of TIA.[7].
References
  1. SAHNI R, WEINBERGER J. Management of intracerebral hemorrhage Vasc Health Risk Manag [online] 2007 Oct, 3(5):701-709 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2291314
  2. NOUH AMRE, REMKE JESSICA, RULAND SEAN. Ischemic Posterior Circulation Stroke: A Review of Anatomy, Clinical Presentations, Diagnosis, and Current Management. Front. Neurol. [online] 2014 April [viewed 06 October 2014] Available from: doi:10.3389/fneur.2014.00030
  3. HAMILTON W, KERNICK D. Clinical features of primary brain tumours: a case-control study using electronic primary care records Br J Gen Pract [online] 2007 Sep 1, 57(542):695-699 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2151783
  4. VINNARD C, MACGREGOR RR. Tuberculous Meningitis in HIV-Infected Individuals Curr HIV/AIDS Rep [online] 2009 Aug, 6(3):139-145 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131531
  5. GELFAND A. A., FULLERTON H. J., GOADSBY P. J.. Child Neurology: Migraine with aura in children. Neurology [online] December, 75(5):e16-e19 [viewed 06 October 2014] Available from: doi:10.1212/WNL.0b013e3181ebdd53
  6. RUCHALSKI KATHLEEN, HATHOUT GASSER M.. A Medley of Midbrain Maladies: A Brief Review of Midbrain Anatomy and Syndromology for Radiologists. Radiology Research and Practice [online] 2012 December, 2012:1-11 [viewed 06 October 2014] Available from: doi:10.1155/2012/258524
  7. NADARAJAN V., PERRY R. J., JOHNSON J., WERRING D. J.. Transient ischaemic attacks: mimics and chameleons. Practical Neurology [online] December, 14(1):23-31 [viewed 06 October 2014] Available from: doi:10.1136/practneurol-2013-000782

Investigations - for Diagnosis

Fact Explanation
MRI Brain Benedikt syndrome diagnosis is suspected mainly by clinical history and examination. Then go for investigations. Diffusion weighted imaging (DWI) is a common form of MRI that has been used. It will show involvement of superior cerebellar peduncle and/or red nucleus, as well as the oculomotor fascicle.And it is useful to exclude certain other pathology such as ICH, ischemia, Tuberculous meningitis, cavernous sinus thrombosis ect..[1],[2],[3].
CT brain Even though CT not well differentiated the mid brain nuclei and fiber tracts they are useful in assessment of visible mid brain anatomy and related pathology. CT is also useful in exclusion of certain other diseases mentioned under Differential diagnosis.[1].
CSF analysis It plays a key role in diagnosis of Tuberculous Meningitis which is one of the differential diagnosis. It will show lymphocytic pleocytosis, with an elevated protein and low glucose levels.[3].
References
  1. RUCHALSKI KATHLEEN, HATHOUT GASSER M.. A Medley of Midbrain Maladies: A Brief Review of Midbrain Anatomy and Syndromology for Radiologists. Radiology Research and Practice [online] 2012 December, 2012:1-11 [viewed 06 October 2014] Available from: doi:10.1155/2012/258524
  2. NOUH AMRE, REMKE JESSICA, RULAND SEAN. Ischemic Posterior Circulation Stroke: A Review of Anatomy, Clinical Presentations, Diagnosis, and Current Management. Front. Neurol. [online] 2014 April [viewed 06 October 2014] Available from: doi:10.3389/fneur.2014.00030
  3. VINNARD C, MACGREGOR RR. Tuberculous Meningitis in HIV-Infected Individuals Curr HIV/AIDS Rep [online] 2009 Aug, 6(3):139-145 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3131531

Investigations - Fitness for Management

Fact Explanation
Full blood count FBc like basic blood tests are performed to rule out infections.[1].
Blood glucose level Random blood sugar level should be test for the assessment of DM causing hypo or hyperglycemia. [1].
Serum electrolytes Carried out to find whether there is associated electrolyte disturbances.[1].
Blood urea and serum creatinine Carried out as a routine laboratory investigation to assess renal functions.[1].
ECG Used to diagnose whether there is ongoing cardiac ischemia or other cardiac pathology.[1].
References
  1. PRASAD KAMESHWAR, PADMA MV, KHURANA DHEERAJ, KAUL SUBHASH, GORTHI SP, BAKSHI ASHA. Stroke management. Ann Indian Acad Neurol [online] 2011 December [viewed 06 October 2014] Available from: doi:10.4103/0972-2327.83084

Management - General Measures

Fact Explanation
Adimit,assessment of airway breathing ,circulation and other relevant examinations Admit the patient to a multidisciplinary stroke unit. After taking a brief history have to go quickly for examination starting from ABC (airway, breathing, circulation) and manage them properly. Mean time look for blood pressure, oxygen saturation, sign of carotid bruits, peripheral pulses, cardiac auscultation, and if there are any serious abnormalities try to correct them and maintain good saturation by providing oxygen via mask[1].
Assessment of GCS and neuroimagine Quickly assess the GCS .Mean time look for head trauma and signs of seizures such as tongue laceration, and if the GCS is low go for relevant management options.Brain imaging have to be performed immediately for patients with persistent neurological symptoms.[1].
Thrombolytic theraphy When CT brain excludes the presence of hemorrhage, can go for thrombolitic theraphy. Tissue plasminogen activator such as alteplase can use if present early with acute ischemic stroke.150 mg of aspirin should be given to all ischemic stroke patients immediately after brain imaging has excluded intracranial hemorrhage. It should be continued until 2 weeks after the onset of stroke symptoms. And antiplatelet or anticoagulant agent is started for secondary prevention. Proton pump inhibitors can be used if patient developed dyspepsia to Asprin. [1].
Antithrombotic or fibrinolytic therapy in ICH If ICH occurs due to IV heparin, normalization of a-PTT have to be carried out with antidote called protamine sulphate. if there is a warfarin related ICH should be managed with vitamin K or fresh frozen plasma (FFP) . If the ICH is related to thrombolysis, it should be treated with infusion of platelets. [1].
Neurosurgery Neurosurgery is occasionally needed in case of massive ICH.[1].
Supportive care After patient get recover from the acute event ask them to change the posture, siting, standing and walking with caution in order to prevent secondary complications. Assess the swallowing by bedside water swallow test. Can introduce nasogastric tube if there is a swallowing difficulty.[1].
Early mobilization Passive full range-of-motion exercises for paralyzed limbs should be started with in first 24 hours. They should be referred to physiotherapist or rehabilitation team.[1].
Nutritional support Nutritional assessment should be carried out with in 48h of admission.Consider nutritional support in malnourished patients.[1].
Prophylactic anticoagulant therapy Patients with paralyzed legs due to ischemic stroke should be given either standard heparin (5000 units subcutaneous b.d.) or LMW heparin in order to prevent deep vein thrombosis.[1].
Bladder bowel care Indwelling catheter can be used because patient is having hemiparesis and difficult to walk to the toilet. Use oral laxatives and maintain good fluid intake in order to overcome constipation.[1].
References
  1. PRASAD KAMESHWAR, PADMA MV, KHURANA DHEERAJ, KAUL SUBHASH, GORTHI SP, BAKSHI ASHA. Stroke management. Ann Indian Acad Neurol [online] 2011 December [viewed 06 October 2014] Available from: doi:10.4103/0972-2327.83084

Management - Specific Treatments

Fact Explanation
Antiplatelet therapy All patients with ischemic stroke should take anti platelet therapy for secondary prevention. Aspirin (30-300 mg/day) or combination of aspirin (25 mg) with extended release dipyridamole (200 mg) twice or clopidogrel (75 mg OD) are the initially used anti platelet therapy.[1].
Anticoagulation Used if there is an associated AF or patients with ischemic stroke associated with mitral valve disease, prosthetic heart valves, or even within 3 months of MI. Heparin and warfarin can be used.[1].
Blood pressure lowering Useful in secondary prevention. Try to maintain BP less than 130/80 mmHg with the help of anti hypertensive drugs.[1].
Lipid lowering therapy All patients with ischemic stroke should be treated with a statin for secondary prevention,if they have a total cholesterol of > 200 mg%, or LDL cholesterol > 100 mg%. Try to maintain total cholesterol below 200mg/dl and LDL below 100mg/dl.[1].
Life style modification Ask them to cessation of smoke if they are already smoking. Ask to do regular aerobic exercise at least 30 minutes per day. Advice them to take healthy diet which contain low fat and inform about safe level of alcohol.[1].
Nonsurgical conservative treatment of ptosis Those treatment methods include eye-putti ,eyelash glue and glasses which made with a crutch attachment to hold up the lid.[2].
Levodopa Studies suggest that levodopa which act as precursor to the neurotransmitters such as dopamine can use to treat tremors in benedikt syndrome.[4],[3].
Deep brain stimulation Deep brain stimulation may provide relief from some symptoms of Benedikt syndrome, specially the tremors associated with the disorder.[3].
References
  1. PRASAD KAMESHWAR, PADMA MV, KHURANA DHEERAJ, KAUL SUBHASH, GORTHI SP, BAKSHI ASHA. Stroke management. Ann Indian Acad Neurol [online] 2011 December [viewed 06 October 2014] Available from: doi:10.4103/0972-2327.83084
  2. KIM SOO YEON, PARK HYE KYUNG, SONG DAE HEON, CHUNG MYUNG EUN, KIM YOUNG MOON, WOO JAE HYUN. Management of Severe Bilateral Ptosis in a Patient With Midbrain Infarction: A Case Report. Ann Rehabil Med [online] 2013 December [viewed 06 October 2014] Available from: doi:10.5535/arm.2013.37.6.891
  3. WOO JH, HONG BY, KIM JS, MOON SH, KIM SY, HAN HY, PARK DY, LIM SH. Holmes Tremor After Brainstem Hemorrhage, Treated With Levodopa Ann Rehabil Med [online] 2013 Aug, 37(4):591-594 [viewed 06 October 2014] Available from: doi:10.5535/arm.2013.37.4.591
  4. FUJIEDA T, YAMAUCHI T, TAKAHASHI S, MOROJI T. Letter: Effect of levodopa on tremor in Benedikt's syndrome. Br Med J [online] 1974 Mar 9, 1(5905):456-457 [viewed 06 October 2014] Available from: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1633264