Secondary Logo

Journal Logo

RFS – Clinical Vignette

Case Report

Fluctuating Mental Status and New Paradoxical Left Hemispatial Neglect During Inpatient Rehabilitation for Left Temporo-Occipital Intracerebral Hemorrhage With Intraventricular Hemorrhage

Weppner, Justin DO; Meriggi, Jenna DO; Franzese, Kevin DO

Author Information
American Journal of Physical Medicine & Rehabilitation: June 2020 - Volume 99 - Issue 6 - p 562-565
doi: 10.1097/PHM.0000000000001293


A 61-yr-old man with a medical history significant for an automatic implantable cardioverter defibrillator placement for a left bundle branch block and Budd-Chiari syndrome of unknown etiology (on chronic warfarin therapy) was admitted to the inpatient rehabilitation unit, after a spontaneous left temporo-occipital intracerebral hemorrhage (ICH) with intraventricular hemorrhage (IVH) secondary to supratherapeutic international normalized ratio of 4 (goal = 2–3) (Fig. 1). Warfarin was reversed with fresh frozen plasma and vitamin K, and an external ventricular drain (EVD) was placed. On acute hospital day (HD) 2, he underwent digital subtraction angiography, which revealed no aneurysm or vascular anomaly to explain the bleeding and no cerebral vasospasm. The 13-day acute hospital course was complicated by delirium, ileus, hyponatremia, and difficulty weaning off the EVD. The EVD was removed on acute HD 12; he was then monitored for 24 hrs before transferring to the inpatient rehabilitation unit for comprehensive rehabilitation.

A, Noncontrast head CT on acute HD 1 demonstrated an ICH centered in the posterior left temporo-occipital region (approximately 6.9 × 3.6 cm) with surrounding vasogenic edema. B, Noncontrast head CT on HD 1 shows the ICH with extension into the ventricular system with IVH. C and D, Noncontrast head CT on rehabilitation HD 3, a fortnight after initial noncontrast CT scan, demonstrates a subacute left temporo-occipital hematoma with a decreasing mass (compared with panels A and B).

During admission at the rehabilitation unit, the patient’s vital signs were stable, and he was alert and oriented to self, place, and year. He was able to follow simple commands, his cranial nerves II–XII were grossly intact, he had full muscle strength of the bilateral upper and lower limbs, and he demonstrated no visuospatial neglect with no extinction on double simultaneous stimulation. To further assess for visuospatial neglect, a cancellation task was performed during initial the therapy evaluation in which the patient had to find and cancel target items that were distributed on an A4-sized sheet of paper. Medications included daily doses of aspirin (81 mg), atorvastatin (40 mg), enoxaparin (40 mg), lisinopril (10 mg), and melatonin (3 mg) at night.

On inpatient rehabilitation HD 3, during the team’s interdisciplinary conference, the therapy team noted that he exhibited a new paradoxical left hemispatial neglect, which did not anatomically correspond with the diagnosis of left ICH with IVH. He was reassessed, and his vital signs were unremarkable. On physical examination, he seemed drowsy and required verbal and tactile stimulation by the examiner to stay awake. He was oriented to person only, which was a decline from his orientation to person, place, and year earlier that same morning. Moreover, he demonstrated difficulty following simple commands without mimicking. A new left hemispatial neglect was noted on the double simultaneous stimulation with right gaze preference. The patient was not able to participate in manual muscle testing or cranial nerve examination. This case study conforms to all CARE guidelines and reports the required information accordingly (see Supplemental Checklist, Supplemental Digital Content 1,

In summary, our patient with a history of left ICH with IVH now presented with fluctuating mental status, a new paradoxical left hemispatial neglect, and right gaze preference. What is the differential diagnosis for this patient?


The list of differential diagnoses for a patient with new neurologic impairment and decline in mental status would first include worsening of ICH, transient ischemic attack, acute ischemic stroke, or new intracranial hemorrhage. To evaluate for these abnormalities, a noncontrast computed tomography (CT) scan of the brain can be performed to evaluate for worsening of ICH or acute intracranial bleeding. The ventricles can also be assessed by a noncontrast head CT scan to evaluate for hydrocephalus. If the noncontrast head CT scan does not reveal any acute abnormalities, it may be followed by a CT angiogram to evaluate for cerebral vasospasm or vascular abnormality and a magnetic resonance imaging (MRI) scan of the brain to evaluate for acute ischemic stroke, which may not appear on a noncontrast CT scan. If the MRI scan is contraindicated, a CT perfusion scan may be used instead to assess for ischemia.

While awaiting imaging, additional evaluations and testing should be considered. Adverse effects of medications could potentially cause mental status changes, and new or sedating medications should be reviewed and considered as potential causes. Vital signs including pulse oximetry can also provide valuable information when considering the differential diagnosis, as hypoxia could potentially cause an altered mental status. Temperature, heart rate, and respiratory rate combined with a complete blood count may assist in identifying potential infectious complications, such as sepsis, encephalitis, meningitis, and meningoencephalitis. A point-of-care glucose test may be conducted quickly at the bedside to assess for hypo or hyperglycemia. Additional laboratory evaluations may be ordered to assess for electrolyte abnormalities, such as hyponatremia, hypernatremia, hypocalcemia, acute kidney failure, uremia, and hyperammonemia.

Seizure activity may result in an altered mental status, and a spot electroencephalogram (EEG) may be performed to evaluate for seizures. If the diagnostic evaluations are uninformative with no acute abnormalities on brain imaging, a lumbar puncture could be considered for a complete evaluation for meningitis and hydrocephalus. Diagnoses of exclusion, such as pseudoseizure, conversion disorder, psychosis, and delirium, should be considered only when other diagnoses are ruled out (Table 1).

Differential diagnosis for a patient with a history of left intracerebral hemorrhage, now presenting with fluctuating mental status, new paradoxical left hemispatial neglect, and right gaze preference

Given the differential diagnosis, what laboratory tests or radiologic imaging should be ordered for further evaluation?


The patient’s medication was reviewed. He had no new medications or sedatives. A point-of-care glucose test revealed normal blood glucose levels. As previously mentioned, the brain MRI was contraindicated in the setting of automatic implantable cardioverter defibrillator.

A noncontrast head CT scan was ordered to evaluate the progression or worsening of ICH. Computed tomography angiography was ordered to evaluate vascular abnormalities. Finally, a CT perfusion scan was ordered to assess for ischemia. Unfortunately, five critically ill trauma patients were queued for CT scans, and therefore, a CT machine was not available for approximately 50 mins. In the meantime, laboratories were drawn including a complete blood count, comprehensive metabolic panel, serum ammonia, and coagulopathy panel, and the patient was escorted for an EEG. A spot EEG showed a well-developed, symmetric, rhythmical 8- to 9-Hz posterior dominant rhythm that attenuated with eye opening. The background was continuous, spontaneously variable, and appropriately reactive. Electroencephalograms while the patient was awake and asleep showed no evidence of epileptiform discharges, seizures, or focal abnormalities.

After the EEG, the CT machine became available, and the patient was escorted directly to the radiology department. Noncontrast head CT was performed to evaluate the progression or worsening of ICH, followed by CT angiography to evaluate for vascular abnormality and a CT perfusion scan to assess for ischemia. Noncontrast head CT revealed maturing subacute left temporo-occipital ICH with no new interval hemorrhage or acute infarct (Fig. 1). Ventricles were stable in size without signs of hydrocephalus. The CT angiogram revealed diminutive supraclinoid internal carotid arteries and carotid termini with relative diminutive caliber of the bilateral proximal A1 and M1 segments, which was consistent with a cerebral vasospasm. Computed tomography perfusion showed reduced cerebral volume corresponding to the recent left ICH with no additional areas of conspicuous asymmetry on perfusion maps. The time from initial evaluation for decline to diagnosis of cerebral vasospasm was approximately 121 mins. A physician escorted the patent to the EEG laboratory and radiology, and upon physical examination, the patient remained stable with no further decline noted on serial examinations.

The laboratories that were ordered revealed normal sodium, potassium, chloride, blood urea nitrogen, creatinine, calcium, alanine aminotransferase, aspartate amino transferase, and serum ammonia levels. With normal serum ammonia and liver function tests, symptomatic Budd-Chiari syndrome was unlikely to be the cause of his symptoms. He did not have coagulopathy that could worsen ICH with a prothrombin time of 14.2 secs, international normalized ratio of 1.1, and platelet count of 182 × 109/L. His white blood cell count was unremarkable, and together with normal vital signs, an infectious process was unlikely.

Considering these imaging findings, what specialty referrals would you make and how would you manage this patient?

Neurosurgery was consulted for angiography, and the neurology stroke service was consulted for postprocedure care and management. He was transferred back to acute care for subsequent digital subtraction angiography, which revealed a severe flow-limiting vasospasm of the bilateral internal carotid arteries and bilateral A1 and M1 segments that was worse on the right side when compared with the left side. He received intraluminal verapamil injected through the angiography catheter directed at the vasospasm followed by placement of an EVD, which improved his mental status and resolved the left-sided neglect. He was transitioned to oral nimodipine for vasospasm treatment and prevention. The EVD was removed on acute readmission HD 5, and he returned to inpatient rehabilitation after a week of acute care management and cerebral vasospasm monitoring. Subsequently, he was discharged to a skilled nursing facility for continued rehabilitation and eventually discharged home at a modified independent level of function.

What can we learn from the diagnosis, treatment, and management of this patient?

This was a case of fluctuating mental status, a new paradoxical left hemispatial neglect, and right gaze preference in an ICH patient with IVH. The severe flow-limiting vasospasm of the internal carotid arteries and A1 and M1 segments caused reversible cerebral ischemia, thereby leading to left hemispatial neglect. The hemispatial neglect was contralateral to the damaged hemisphere, and the left temporo-occipital intracerebral hemorrhage that the patient presented with to rehabilitation would not explain his new symptoms. Once the treatment team reported findings of left hemispatial neglect with discordant radiologic imaging of left-sided ICH, a wide differential diagnosis was considered. Additional imaging and laboratory evaluations were conducted, identifying a cerebral vasospasm that could have resulted in bilateral irreversible cerebral ischemia. A team approach is the hallmark of rehabilitation, and interdisciplinary teams emphasize open, honest, and direct communication, helping advance safe and effective patient care. This patient’s fluctuating presentation further underscores the importance of team communication as otherwise it may have dangerously progressed before a definitive diagnosis.

Neuroimaging has revolutionized health care; however, advanced imaging studies must be interpreted within the context of physical examination findings, and overreliance on neuroimaging should be avoided. This case demonstrates the importance of correlating physical examination findings with radiographic anatomy, and when the two findings are discordant, further investigations are necessary. Physical examination findings can make a strong case for the presence of a pathologic process, despite not being observed in the current radiologic imaging, as there are limits to each imaging technique.

Intracerebral hemorrhage with IVH portends a worse prognosis and increases the 30-day mortality (43%–80%) compared with ICH without IVH (9%). Increased ICH volumes can foretell poorer outcomes. 1,2 One theory is that the extension of blood into the subarachnoid space might mirror the same pathways associated with subarachnoid hemorrhage (SAH). Cerebral vasospasm is a well-known expected complication of SAH. Clinically significant cerebral vasospasms affect 20%–30% of patients with SAH. 3,4 The principal pathophysiological mechanism is proposed to be facilitated by circulating heme products within the cerebrospinal fluid; thus, ICH patients with IVH may also be at risk for developing cerebral vasospasms. 3 Although the true incidence of cerebral vasospasm secondary to ICH with IVH has not been well described, a study on 115 patients with ICH reported an incidence of 5.6%. 5 In the setting of SAH, vasospasm usually occurs at HD 3–14, with a peak incidence at approximately 7 days after the original event. 6 In the present case, it was unclear when the vasospasm began. It occurred sometime within the 15 days between the negative (acute HD 2) and positive (inpatient rehabilitation HD 3) angiograms, and if the cerebral vasospasm occurred on inpatient rehabilitation HD 3, he would have been outside the expected window for a cerebral vasospasm, because vasospasm was not be expected in this timeframe during acute rehabilitation.

External ventricular drain placement has a protective effect against the development of cerebral vasospasms, with a three-fold decreased incidence in SAH patients with an EVD. 7 We hypothesized that the protective nature of the EVD, which helps eliminate subarachnoid blood and heme products, may have delayed the onset of the cerebral vasospasm in this patient until 3 days after EVD removal.

When physical examination findings are conflicting with the expected findings based on radiographical anatomy, further evaluation is warranted, and a broad differential diagnosis should be considered. Strong interdisciplinary teamwork is a hallmark of effective rehabilitation management and encourages all team members to feel comfortable in reporting concerns noted on therapy, whereas nursing evaluations are also vital. Active listening from the rehabilitation physician and addressing concerns noted by the therapy team can improve the effectiveness of medical care provided in the rehabilitation unit. Although ICH is not commonly associated with cerebral vasospasm, practitioners treating patients with ICH should be aware of the risk of cerebral vasospasm associated with IVH. If a patient with ICH and IVH experiences clinical deterioration during inpatient rehabilitation, then cerebral vasospasm should be considered in the differential diagnosis.


1. Morgan T, Awad I, Keyl P, et al: Preliminary report of the clot lysis evaluating accelerated resolution of intraventricular hemorrhage (CLEAR-IVH) clinical trial. Acta Neurochir Suppl 2008;105:217–20
2. Tuhrim S, Horowitz DR, Sacher M, et al: Volume of ventricular blood is an important determinant of outcome in supratentorial intracerebral hemorrhage. Crit Care Med 1999;27:617–21
3. Kassell NF, Sasaki T, Colohan AR, et al: Cerebral vasospasm following aneurysmal subarachnoid hemorrhage. Stroke 1985;16:562–72
4. Schmidt JM, Wartenberg KE, Fernandez A, et al: Frequency and clinical impact of asymptomatic cerebral infarction due to vasospasm after subarachnoid hemorrhage. J Neurosurg 2008;109:1052–9
5. Kiphuth IC, Huttner HB, Breuer L, et al: Vasospasm in intracerebral hemorrhage with ventricular involvement: a prospective pilot transcranial Doppler sonography study. Cerebrovasc Dis 2011;32:420–5
6. Kiser TH: Cerebral vasospasm in critically iii patients with aneurysmal subarachnoid hemorrhage: does the evidence support the ever-growing list of potential pharmacotherapy interventions? Hosp Pharm 2014;49:923–41
7. Della Pepa GM, Scerrati A, Albanese A, et al: Protective effect of external ventricular drainage on cerebral vasospasm. A retrospective study on aneurysmal SAH treated endovascularly. Clin Neurol Neurosurg 2014;124:97–101

Cerebral Vasospasm; Intraventricular Hemorrhage; Intracerebral Hemorrhage; Brain Injury Medicine

Supplemental Digital Content

Copyright © 2020 Wolters Kluwer Health, Inc. All rights reserved.