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BACKGROUND AND PURPOSE: Anoxic brain injury is a result of prolonged hypoxia. We sought to describe the nonquantitative arterial spin-labeling perfusion imaging patterns of anoxic brain injury, characterize the relationship of arterial spin-labeling and DWI, and evaluate the normalized diffusion-to-perfusion ratio to differentiate patients with anoxic brain injury from healthy controls. MATERIALS AND METHODS: We identified all patients diagnosed with anoxic brain injuries from 2002 to 2019. Twelve ROIs were drawn on arterial spin-labeling with coordinate-matched ROIs identified on DWI. Linear regression analysis was performed to examine the relationship between arterial spin-labeling perfusion and diffusion signal. Normalized diffusion-to-perfusion maps were generated using a custom-built algorithm. RESULTS: Thirty-five patients with anoxic brain injuries and 34 healthy controls were identified. Linear regression analysis demonstrated a significant positive correlation between arterial spin-labeling and DWI signal. By means of a combinatory cutoff of slope of >0 and R2 of > 0.78, linear regression using arterial spin-labeling and DWI showed a sensitivity of 0.86 (95% CI, 0.71–0.94) and specificity of 0.82 (95% CI, 0.66–0.92) for anoxic brain injuries. A normalized diffusion-to-perfusion color map demonstrated heterogeneous ratios throughout the brain in healthy controls and homogeneous ratios in patients with anoxic brain injuries. CONCLUSIONS: In anoxic brain injuries, a homogeneously positive correlation between qualitative perfusion and DWI signal was identified so that areas of increased diffusion signal showed increased ASL signal. By exploiting this relationship, the normalized diffusion-to-perfusion ratio color map may be a valuable imaging biomarker for diagnosing anoxic brain injury and potentially assessing BBB integrity.

BRASH (bradycardia, renal failure, atrioventricular [AV] nodal blocking medications, shock, hyperkalemia) syndrome describes the phenomenon of profound bradycardia from a combination of hyperkalemia and use of AV nodal blocking medication with underlying renal injury. We present a case of BRASH syndrome in a patient on chronic beta-blocker therapy for his coronary artery disease who presented with life-threatening hyperkalemia and acute renal failure. Due to failure in early recognition and superimposed effect with further beta-blocker dosing, the patient developed profound bradycardia and later went into pulseless electrical activity cardiac arrest requiring cardiopulmonary resuscitation. Metabolic derangements and bradycardia later resolved with medical management, but unfortunately, the patient developed diffuse anoxic brain injury after the cardiac arrest and was declared brain dead.

Background Electroencephalography (EEG) is commonly used after cardiac arrest. Burst suppression with identical bursts (BSIB) has been reported as a perfectly specific predictor of poor outcome but published case series are small. We describe two patients with BSIB who awakened from coma after cardiac arrest. Methods We identified two out-of-hospital cardiac arrest (OHCA) patients with coma and BSIB. We determined the etiology of arrest, presenting neurological examination, potential confounders to neurological assessment, neurodiagnostics and time to awakening. We reviewed and interpreted EEGs using 2021 American Clinical Neurophysiology Society guidelines. We quantified identicality of bursts by calculating pairwise correlation coefficients between the first 500 ms of each aligned burst. Results In case one we present a 62-year-old man with OHCA secondary to septic shock. EEG showed burst suppression pattern, with bursts consisted of high amplitude generalized spike waves in lock-step with myoclonus (inter-burst correlation = 0.86). He followed commands 3 days after arrest, when repeat EEG showed a continuous, variable and reactive background without epileptiform activity. Case two was a 49-year-old woman with OHCA secondary to polysubstance overdose. Initial EEG revealed burst suppression with high amplitude generalized polyspike-wave bursts with associated myoclonus. She followed commands on post-arrest day 4, when repeat EEG showed a continuous, variable and reactive background with frequent runs of bifrontal predominant sharply contoured rhythmic delta activity. Conclusion These cases highlight the perils of prognosticating with a single modality in comatose cardiac arrest patients.

Trauma by electricity imposes mechanical, electrical, and thermal forces on the human body. Often, the delicate cardiac electrophysiology is disrupted causing dysrhythmia and subsequent cardiac arrest. Anoxic brain injury (ABI) is the most severe consequence and the main cause of mortality following cardiac arrest. Establishing a working protocol to treat patients who are at risk for ABI after suffering a cardiac arrest is of paramount importance. There has yet to be sufficient exploration of combination therapy of therapeutic hypothermia (TH) and progesterone as a neuroprotective strategy in patients who have suffered cardiac arrest after electric shock. The protocol required TH initiation upon transfer to the ICU with a target core body temperature of 33°C for 18 hours. This was achieved through a combination of cooling blankets, ice packs, chilled IV fluids, nasogastric lavage with iced saline, and intravascular cooling devices. Progesterone therapy at 80-100 mg intramuscularly every 12 hours for 72 hours was initiated shortly after admission to the ICU. We present a case series of three patients (mean age = 29.3 years, mean presenting Glasgow Coma Score = 3) who suffered ventricular fibrillation (VF) cardiac arrest from non-lightning electric shock, and who had considerably improved outcomes following the TH-progesterone combination therapy protocol. The average length of stay was 13.7 days. The cases presented suggest that there may be a role for neuroprotective combination therapy in post-resuscitation care of VF cardiac arrest. While TH is well documented as a neuroprotective measure, progesterone administration is a safe therapy with promising, albeit currently inconclusive, neuroprotective effect. Future protocols involving TH and progesterone combination therapy in these patients should be further explored.

Seesaw nystagmus (SSN) is a rare ocular manifestation characterized by cyclic movement of the eyes with a conjugate torsional component and a disjunctive vertical component. We present a 29-year-old woman with alcohol withdrawal seizure resulting in anoxic brain injury secondary to respiratory failure. On examination, she had multifocal myoclonus, dystonia, and SSN (video). The proposed mechanism is inactivation of the torsional eye-velocity integrator, the interstitial nucleus of Cajal, with sparing of the torsional fast-phase generator, the rostral interstitial nucleus of MLF. This is a unique case of Lance Adams syndrome1,2 combined with SSN.

We aimed to investigate the factors that modulate the extent of QTc prolongation and potential arrhythmogenic consequences during mild therapeutic hypothermia (MTH).We studied 205 patients after out-of-hospital cardiac arrest (131 underwent MTH). QTc was measured at baseline, 3h, 6h, 12h, 24h (end of hypothermia), 48h and 72h, and ventricular arrhythmias quantified.During MTH, the QTc interval increased progressively peaking at 12h (mean increase 42ms, 95% CI 30-55). There was a strong gender effect (P0.001) and a significant gender-by-MTH interaction (P=0.004). At 12h, the QTc interval was markedly longer in women as compared with men (mean difference 50ms [95% CI 27-73]. Anoxic brain injury (P=0.002) was also positively associated with QTc prolongation. The risk for ventricular arrhythmic events was not higher with MTH compared with no hypothermia (incidence rate ratio 0.57, 95% CI 0.32-1.02, P=0.06). However, typical cases of Torsade de pointes occurred in association with AV block and LQT2.QTc prolongation during MTH is strongly affected by female gender and moderately by concomitant anoxic brain injury. Although the overall risk for ventricular arrhythmias is not greater with MTH, Torsade de pointes may develop when other contributing factors coexist.

Cardiac arrest is a common cause of coma with frequent poor outcomes. Palliative medicine teams are often called upon to discuss the scope of treatment and future care in cases of anoxic brain injury. Understanding prognostic tools in this setting would help medical teams communicate more effectively with patients’ families and caregivers and may promote improved quality of life overall. This article reviews multiple tools that are useful in determining outcomes in the setting of postarrest anoxic brain injury.

Anoxic brain injury can manifest with various abnormal movements. We describe acute chorea in a young patient with anoxic brain injury due to chlordiazepoxide toxicity who had delayed radiographic lesions in bilateral globus pallidus. Although brain MRI 8days after the anoxic event was unremarkable, repeat brain MRI 15days after the event showed T2 hyperintensities and enhancement within the bilateral globus pallidi. It is possible that MRI brain findings of bilateral basal ganglia lesions may appear later than onset of chorea in anoxic brain injury. However, given the normal brain MRI in between, other etiologies cannot be excluded entirely.

A 63-year-old woman was hospitalized for rehabilitation from the aftereffects of an anoxic brain injury. In addition to a general cognitive decline, agraphia of kana and kanji was noted at the time of admission, which had advanced to agraphia which is dominant in kanji at the time of hospital discharge. Brain magnetic resonance imaging revealed no stroke lesions, and brain perfusion scintigraphy found a decreased blood flow in the bilateral parietal lobes. We hereby report on this case because case reports on agraphia caused by anoxic brain injury are extremely rare.

Objective Recognition of potential for neurological recovery in patients who remain comatose after cardiac arrest is challenging and strains clinical decision making. Here, we utilize an approach that is based on physiological principles underlying recovery of consciousness and show correlation with clinical recovery after acute anoxic brain injury. Methods A cohort study of 54 patients admitted to an Intensive Care Unit after cardiac arrest who underwent standardized bedside behavioral testing (Coma Recovery Scale – Revised [CRS-R]) during EEG monitoring. Blinded to all clinical variables, artifact-free EEG segments were selected around maximally aroused states and analyzed using a multi-taper method to assess frequency spectral content. EEG spectral features were assessed based on pre-defined categories that are linked to anterior forebrain corticothalamic integrity. Clinical outcomes were determined at the time of hospital discharge, using Cerebral Performance Categories (CPC). Results Ten patients with ongoing seizures, myogenic artifacts or technical limitations obscuring recognition of underlying cortical dynamic activity were excluded from primary analysis. Of the 44 remaining patients with distinct EEG spectral features, 39 (88%) fit into our predefined categories. In these patients, spectral features corresponding to higher levels of anterior forebrain corticothalamic integrity correlated with higher levels of consciousness and favorable clinical outcome at the time of hospital discharge (P = 0.014). Interpretation Predicted transitions of neocortical dynamics that indicate functional integrity of anterior forebrain corticothalamic circuitry correlate with clinical outcomes in postcardiac-arrest patients. Our results support a new biologically driven approach toward better understanding of neurological recovery after cardiac arrest.

EEG testing is frequently ordered when there is a clinical suspicion of seizures or when a patient is placed on a hypothermia protocol following anoxic brain injury. Hypoxic ischemic encephalopathy...

Introduction Paroxysmal sympathetic hypersensitivity (PSH) has become more frequently recognized in patients with severe neurological brain injury. Left untreated, PSH has been associated with poor neurological outcomes. Currently, most therapeutic options are circumstantial with evidence stemming from subjective case reports. Case series Two young females were admitted after cardiac arrest and found to have anoxic brain injury with subsequent PSH. Initial treatment was targeted at relief of the hyperadrenergic symptoms, which included bromocriptine, propranolol, opioids and benzodiazepines. These therapies were minimally effective, and the patients remained comatose. After initiation of enteral baclofen treatment, they exhibited drastic reduction of PSH symptoms and became alert and interactive. After a 6-week hospital stay, they were both discharged to long-term rehabilitation centers. Conclusion This case series reviews the current therapies used for PSH and discusses 2 patients with uncontrolled PSH secondary to anoxic brain injury. Both patients arose from coma and had significant symptomatic improvement with enteral baclofen treatment. Thus, enteral baclofen should be considered as a primary treatment for PSH to prevent sustained symptoms and prolonged hospitalizations.

The severity of neuronal damages in comatose patients following anoxic brain injury can be probed by evoked auditory responses. However, it remains challenging to predict the return to full consciousness of post-anoxic coma of hospitalized patients. We presented here a method to predict the return to consciousness based on the analysis of periodic responses to auditory stimulations, recorded from surface cranial electrodes. The input data are event-related potentials (ERPs), recorded non-invasively with electro-encephalography (EEG). We extracted several novel features from the time series responses in a window of few hundreds of milliseconds from deviant and non-deviant auditory stimulations. We use these features to construct two-dimensional statistical maps, that show two separated clusters for recovered (conscience) and deceased patients, leading to a high classification success as tested by a cross-validation procedure. Finally, using Gaussian, K-neighborhood and SVM classifiers, we construct probabilistic maps to predict the outcome of post-anoxic coma. To conclude, statistics of deviant and non-deviant responses considered separately provide complementary and confirmatory predictions for the outcome of anoxic coma.

Therapeutic hypothermia (TH) is clinically used to improve neurologic outcomes in patients with anoxic brain injury after cardiopulmonary resuscitation (CPR). For patients that regress and become organ donors after neurologic determination of death (DNDDs), the impact of TH received before determination of death on organ donation outcomes remains unknown. A prospective observational study of all adult DNDDs that received CPR and had anoxia as a cause of death from March 2013 to December 2014 was conducted across 20 organ procurement organizations (OPOs) in the United States. Main outcome measures included organs transplanted per donor (OTPD), specific organ transplantation rates, and recipient graft outcomes. One thousand ninety eight DNDDs met inclusion criteria, with 46% having received TH before determination of death. DNDDs with hypothermia before death had a similar number of OTPD (2.74 vs. 2.69

We have seen a patient with a profound, isolated, and quite selective deficit in proverb interpretation-aproverbia. The patient presented to us after an anoxic brain injury with aproverbia. Interestingly, the aproverbia appeared to be premorbid to the presenting event. Furthermore, the patient had no brain lesion that has been associated or even proposed as a cause of deficit in proverb or metaphor interpretation. The patient did have acute bilateral hippocampi lesions and associated severe anterograde amnesia, but he retained good retrograde memory with which he is able to give good, logical but concrete explanations for proverbs. This case highlights the need, importance, and interest in further neuropsychologic, imaging and functional studies of proverb and interpretation in patients and normal subjects populations.

BACKGROUND: Targeted Temperature Management (TTM) is a class I recommendation for the management of sudden cardiac arrest (SCA) patients with presumed brain injury. We aimed to study trends, predictors and outcomes in SCA patients from a nationally represented US population sample. METHODS: We utilized the National Inpatient Sample from years 2005 to 2014 for the purpose of our study. Patients with SCA and anoxic brain injury were selected using relevant ICD-9 codes. Data were analyzed for trends over the years and key outcomes were assessed. Logistic regression analysis was done to determine predictors of TTM utilization in our study population. RESULTS: A total of 78,465 patients with SCA and anoxic brain injury were identified from January 2005 to December 2014. Out of these, approximately 4,481 (5.7%) patients underwent TTM. Patients that underwent TTM were younger compared to patients without TTM utilization (60.67 vs. 63.27 years, P < 0.01). African Americans, Hispanics and women were less likely to undergo TTM. Myocardial infarction, electrolyte disorders and cardiogenic shock were associated with higher odds of TTM utilization. Sepsis, renal failure and diabetes were associated with underutilization of TTM. Inpatient mortality was higher in patients who did not undergo TTM when compared to patients who underwent TTM (67.30% vs. 65.10%, P < 0.01). CONCLUSIONS: Although TTM utilization increased over our study period, the overall application of TTM was still dismal. Factors that circumvent TTM utilization need to be addressed in future studies so more eligible patients could benefit from this life saving therapy.

BackgroundIt is unknown whether postanoxic cortical and subcortical myoclonus are distinct entities with different prognoses.MethodsIn this retrospective cohort study of 604 adult survivors of cardiac arrest over 8.5 years, we identified 111 (18%) patients with myoclonus. Basic demographics and clinical characteristics of myoclonus were collected. EEG reports, and, when available, raw video EEG, were reviewed, and all findings adjudicated by 3 authors blinded to outcomes. Myoclonus was classified as cortical if there was a preceding, time-locked electrographic correlate and otherwise as subcortical. Outcome at discharge was determined using Cerebral Performance Category.ResultsPatients with myoclonus had longer arrests with less favorable characteristics compared to patients without myoclonus. Cortical myoclonus occurred twice as often as subcortical myoclonus (59% vs 23%, respectively). Clinical characteristics during hospitalization did not distinguish the two. Rates of electrographic seizures were higher in patients with cortical myoclonus (43%, vs 8% with subcortical). Survival to discharge was worse for patients with myoclonus compared to those without (26% vs 39%, respectively), but did not differ between subcortical and cortical myoclonus (24% and 26%, respectively). Patients with cortical myoclonus were more likely to be discharged in a comatose state than those with subcortical myoclonus (82% vs 33%, respectively). Among survivors, good functional outcome at discharge was equally possible between those with cortical and subcortical myoclonus (12% and 16%, respectively).ConclusionsCortical and subcortical myoclonus are seen in every sixth patient with cardiac arrest and cannot be distinguished using clinical criteria. Either condition may have good functional outcomes.

Introduction Serum neuron-specific enolase (NSE) levels have been shown to correlate with neurologic outcome in comatose survivors of cardiac arrest but use of absolute NSE thresholds is limited. This study describes and evaluates a novel approach to analyzing NSE, the NSE ratio, and evaluates the prognostic utility of NSE absolute value thresholds and trends over time. Methods 100 consecutive adult comatose cardiac arrest survivors were prospectively enrolled. NSE levels were assessed at 24, 48, and 72 h post-arrest. Primary outcome was the Glasgow Outcome Score (GOS) at 6 months post-arrest; good outcome was defined as GOS 3–5. Absolute and relative NSE values (i.e. the NSE ratio), peak values, and the trend in NSE over 72 h were analyzed. Results 98 patients were included. 42 (43%) had a good outcome. Five good outcome patients had peak NSE >33 µg/L (34.9–46.4 µg/L). NSE trends between 24 and 48 h differed between outcome groups (decrease by 3.0 µg/L (0.9–7.0 µg/L) vs. increase by 13.4 µg/L (−3.7 to 69.4 µg/L), good vs. poor, p = 0.004). The 48:24 h NSE ratio differed between the good and poor outcome groups (0.8 (0.6–0.9) vs. 1.4 (0.8–2.5), p = 0.001), and a 48:24 h ratio of ≥1.7 was 100% specific for poor outcome. Conclusions The NSE ratio is a unique method to quantify NSE changes over time. Values greater than 1.0 indicate increasing NSE and may be reflective of ongoing neuronal injury. The NSE ratio obviates the need for an absolute value cut-off.

Stroke is a major cause of neurological disability and death in industrialized nations. Therapeutic hypothermia has been shown to protect the brain from ischemia, stroke, and other acute neurological insults at the laboratory level. It has been shown to improve neurological outcome in certain clinical settings including anoxic brain injury due to cardiac arrest and hypoxic-ischemic neonatal encephalopathy. Hypothermia seems to affect multiple aspects of brain physiology and it is likely that multiple mechanisms underlie its protective effect. Understanding the events that occur in the ischemic brain during hypothermia might help lead to an understanding of how to protect the brain against acute injuries.

Central Diabetes Insipidus is often an overlooked complication of cardiopulmonary arrest and anoxic brain injury. We report a case of transient Central Diabetes Insipidus (CDI) following cardiopulmonary arrest. It developed 4 days after the arrest resulting in polyuria and marked hypernatremia of 199 mM. The latter was exacerbated by replacing the hypotonic urine by isotonic saline.

This chapter aims to provide clinicians with an evidence based approach to the principles of management of patients who have suffered anoxic brain injury following cardiac arrest. The diagnosis of anoxic brain injury is discussed, followed by an in depth review of the history and evolution of therapeutic hypothermia and its evolution into targeted temperature management including subsequent maintenance of normothermia. This chapter also provides evidence based recommendations on supportive care and comprehensive multi-system management of patients with anoxic brain injury as well as in-depth review of the current state of the evidence in neurologic prognostication.

Aim of the study: This exploratory study aimed to investigate the psychosocial outcomes for cardiac arrest survivors and explore if there is a greater impact on psychosocial outcome for individuals experiencing anoxic brain injury as a result of the cardiac arrest. Methods: Self-report measures were used to compare the quality of life, social functioning and symptoms of anxiety, depression and posttraumatic stress of individuals with and without anoxic brain injury. Secondary measures of subjective memory and executive difficulties were also used. Fifty-six participants (27 with anoxia, 29 without anoxia) took part in the study between six months and four years after experiencing cardiac arrest. Results: A MANOVA identified a significant difference between the two groups, with the anoxia group reporting more psychosocial difficulties. They reported more social functioning difficulties and more anxiety, depression and post-traumatic stress symptoms. There was, however, no significant difference in self-reported quality of life between the two groups. Conclusion: As the first known study to compare psychosocial outcomes for cardiac arrest survivors experiencing anoxic brain injury with those without anoxia, the current results suggest that cardiac arrest survivors with subsequent acquired brain injury experience more psychosocial difficulties. This could be due to a combination of neuropsychological, social and psychological factors.

Integrated post-resuscitation treatment has improved the outcome of the unconscious patients with cardiac arrest after introduction of the therapeutic hypothermia, which had shown promising results in the two pivotal randomized trials. Early assessment of neurological function and prognostication in these comatose patients has been challenging problem, and the introduction of therapeutic hypothermia made the problem more confusing. Various clinical situations, the results of the clinical neurologic examination, neurophysiologic monitoring including electroencephalography and somatosensory evoked potentials, various biomarkers, and neuroimaging can be used in predicting early prognosis. No single test is allowed to predict the prognosis with certainty, and a multimodal strategy is generally recommended. The previous practice guideline of the American Academy of Neurology in 2006 may not be appropriate anymore in the era of therapeutic hypothermia. In this review, the author introduces various neuromonitoring methods currently used in the therapeutic hypothermia and evaluate the their role in the prognostication with available evidences.

Burst suppression (BS) is an electroencephalogram (EEG) pattern that is characterized by brief bursts of spikes, sharp waves, or slow waves of relatively high amplitude alternating with periods of relatively flat EEG or isoelectric periods. The pattern is usually associated with coma, severe encephalopathy of various etiologies, or general anesthesia. We describe an unusual case of anoxic brain injury in which a BS pattern was seen during behaviorally defined sleep during a routine outpatient EEG study.

Various neurological impairments other than traumatic brain injury (TBI) are routinely encountered in critically ill populations. The more common diseases seen in a non-neurological ICU include acute ischemic stroke, cerebral infections, cerebral vein thrombosis, status epilepticus, anoxic brain injury, brain tumors, primary intracerebral hemorrhage, and aneurysmal subarachnoid hemorrhage. These conditions are potentially devastating and life threatening. However, most of these conditions may be successfully managed using fundamental critical care techniques in combination with expert neurologist consultation. With an awareness of the basic nuances of specific neurological diseases, proper collaborative care can be delivered to these patients in a timely fashion.

Therapeutic hypothermia (TH) is a management option with demonstrated benefit for survivors of cardiac arrest. Unfortunately, the incorporation of TH has been slow. The objective of the article is to review the development of a multidisciplinary TH program at a quaternary referral center. Important issues that presented as barriers to implementation to TH, and the authors’ solution to these, are also presented. Review of patient outcomes after the introduction of the TH program highlights the importance of this therapeutic modality in this common and devastating event.

Permanent neurologic impairment following cardiac arrest is often severely debilitating, even after successful resuscitation. Therapeutic hypothermia decreases anoxic brain injury and subsequent cognitive deficits. Current practice guidelines recommend therapeutic hypothermia in comatose survivors of cardiac arrest. To address the multifacets of therapeutic hypothermia, we assembled a multidisciplinary task force including members from various specialties to create an evidence-based guideline with transparency across disciplines and consistency of care. We describe our institutional guidelines for the initiation and management of induced hypothermia in patients successfully resuscitated from a cardiac arrest.

A 36-year-old woman had severe anoxic brain damage due to a pulmonary embolus during a long airplane flight. She was admitted to the neurology intensive care unit but remained in a coma despite maximal medical therapy. On the ninth day, the family decided to institute comfort measures only. Later, they requested that maximal therapy be resumed, to permit consideration of oocyte retrieval for the purpose of posthumous conception of future offspring. A management decision was made.

To compare the functional outcomes of patients with anoxic brain injury (ABI) and patients with traumatic brain injury (TBI) following inpatient rehabilitation.Retrospective chart review.Data on 68 patients with brain injury (34 with ABI and 34 with TBI) were collected.The ABI and TBI groups were demographically similar, except that patients with ABI were more likely to be married. Both groups significantly improved their function and were similar upon discharge. For the ABI group, there were trends toward a shorter length of stay, increased total FIM efficiency and decreased cost of stay when compared with the TBI group. The patients with ABI tended to be discharged to a sub-acute rehabilitation facility more than those in the TBI group.This study is important because it shows that patients with ABI benefit from inpatient rehabilitation and made significant functional gains comparable to the gains of patients with TBI.

Heterotopic ossification (HO) is the formation of bone in the soft tissue, which exhibits no properties of ossification. Widespread HO is an uncommon condition. We present the findings in an 18-year-old young female who presented with benign bilateral fibroadenoma of the breast. However, she suffered an anoxic brain injury following cardiac arrest and had mechanical ventilation for some weeks. Thereafter, she developed widespread HOs, which were subsequently managed conservatively but required surgery for the ossification around the right hip. The report highlighted the multiplicity of risk factors vis-a-vis the challenges of management. A plan for the future care of this patient in relation to some of the currently available literature has also been highlighted.

Stroke is the third most common cause of death in the Western world, behind heart disease and cancer, and accounts for over half of all neurologic admissions to community hospitals. Spasticity is commonly defined as excessive motor activity characterized by a velocity-dependent increase in tonic stretch reflexes. It is often associated with exaggerated tendon jerks, and is often accompanied by abnormal cutaneous and autonomic reflexes, muscle weakness, lack of dexterity, fatigability, and co-contraction of agonist and antagonist muscles. It is a common complication of central nervous system disorders, including stroke, traumatic brain injury, cerebral palsy, multiple sclerosis, anoxic brain injury, spinal cord injury, primary lateral sclerosis, and hereditary spastic hemiparesis. Leg muscle activation during locomotion is produced by spinal neuronal circuits within the spinal cord, the spinal pattern generator [central pattern generator (CPG)]. For the control of human locomotion, afferent information from a variety of sources within the visual, vestibular, and proprioceptive systems is utilized by the CPGs. Findings of this research can be applied to older adults in longitudinal home care who suffer spasticity caused by stroke.

This chapter addresses the effects of stroke and anoxic brain injury on the tier 1 caregiver and tier supports. First, the neuropathology of various types of strokes and anoxia is reviewed. Family scenarios are employed to address common sequelae of strokes and/or anoxia, specifically, aphasia; cognitive (especially attention, memory, and executive functions) and behavioral deficits as well as vision and motor changes (e.g., hemianopia, visuoperceptual, visuospatial, constructional skills, visual neglect, hemiplegia/hemiparesis, and other movement disorders). A series of psychotherapeutic “helpful hints” are presented for each realm for the caregiver and family to better comprehend and cope with their loved one’s stroke or anoxic symptoms and recovery. An emphasis is placed on new assistive technology that can be incorporated in therapy and at home to compensate for language, cognitive, vision, and motor impairments. This chapter also describes common areas of caregiver angst and disillusionment after stroke or anoxia with a variety of proposed psychoeducational and therapeutic tools to promote adaptation. Some of the unique challenges and useful strategies for spouses are also addressed within this chapter. Finally, an integrative case study is presented, illustrating core concepts and techniques.

Improved cooling technologies (such as newer intravascular cooling devices) may result in earlier attainment of target temperature and even more robust clinical benefits in the management of the survivors of cardiac arrest. Earlier cooling may also be facilitated by the introduction of cooled saline infusions in the emergency room setting, prior to induction of cooling in the intensive care unit. However, there is a need for studies of adjunctive therapies to minimize the risk of medical complications associated with hypothermia, the most serious of which is infection. We strongly believe that larger confirmatory studies might encourage more widespread adoption of therapeutic hypothermia for survivors of cardiac arrest and further studies are also needed to evaluate the utility of this procedure for more expanded indications, including asystole, pulseless electrical activity, and in-hospital arrest in patients without significant comorbidity.

Since the introduction of mild induced hypothermia as a neuroprotective measure in patients after cardiac arrest (CA), there have been numerous questions regarding the validity of previously established prognostication methods (1–3). The concern has been: if hypothermia can improve neurologic outcomes, then perhaps by using older prognostication markers, we have been underestimating the recovery potential of hypothermia-treated patients. An obvious and grave consequence would be misleading the patient’s family members to withdraw care prematurely. Fortunately, several studies published over the past few years have attempted to clarify the validity of early and long-term prognostication markers in patients treated with hypothermia (4–8). In this edition of Critical Care Medicine, Hsu et al adds to the growing body of literature that examines predictors of prognosis in cardiac arrest patients treated with therapeutic hypothermia (9). In their study of patients treated with targeted temperature management (TTM) of 33 to 34°C after cardiac arrest, the authors reported that good Cerebral Performance Category (CPC) scores at hospital discharge predicted longer patient survival. Their study included out-of-hospital and in-hospital post-cardiac arrest patients with both groups demonstrating similar correlations between CPC scores and long-term survival. The important and noteworthy feature of this study is the fact that they looked exclusively at patients treated with hypothermia. This significantly highlights the importance of the research focus on hypothermia and also explains the slightly low sample size as only a fraction of post-cardiac arrest patients are treated with TTM (24.1%, 140/582 in this study) (9). Other studies correlating CPC with long-term survival after cardiac arrest included a mix of patients treated with and without TTM, introducing uncertainty regarding the validity of their results in cooled patients (10, 11). Accounting for the differences in sample size between the studies, the strong correlation between CPC score at discharge and long-term survival was similar in the present study compared to the previous ones. One may not find this similarity between patients treated with or without hypothermia surprising, especially given the recently published large trial that showed no significant benefit of a protocol of mild hypothermia over anti-pyrexia (12). Interestingly, the study by Phelps et al (10), which included a large proportion of patients not treated with TTM (75.3%), had a lower percentage of patients at discharge with CPC score 3 or 4. Though no explanation of the difference is offered by Hsu et al, one possibility is the selection bias of patients treated with TTM. That is, TTM is usually only instituted in patients who remain comatose after resuscitation from a cardiac arrest, thereby selecting out patients with mild to moderate initial cerebral injury. The present study’s choice of using the CPC score as the prognostic marker has its advantages as well as drawbacks (9). The CPC score has been widely used in the cardiac arrest literature, and is relatively easy to estimate and interpret, though typically as an outcome measure (however intermediate) rather than a prognostic marker. The straightforwardness of the scale also makes it simple for family members to understand the meaning of each category. However, the authors’ exclusive use of chart review by one of three abstractors (without the evaluation of inter-rater reliability) as the method for ascertaining CPC scores at hospital discharge calls into question the accuracy of the assigned scores. Additionally, the CPC score is a very broad measure of global function and best used as a measure of outcome. It does not address specific deficits useful for predicting functional outcomes (such as language, memory, or ambulatory function) that other more comprehensive scales assess (13). Most neurologists/intensivists may not wait until discharge to talk with families about prognosis, thus earlier tests and markers should be the focus in future researches. Perhaps more important than the length of a patient’s life, quality has become a key determinant of decisions regarding life-sustaining measures. Essential to every family discussion about prognosis is not only the likelihood of survival, but also an estimate of what that life will look like. One limitation of the study by Hsu et al (9) is that the only outcome measure was the length of survival after hospital discharge. It would have been very interesting and informative to see if there were changes in the CPC scores of the patients over time. In particular, do patients with anoxic brain injury that are discharged from the hospital in an unconscious state (CPC 4) remain so for the rest of their lives? Did some regain consciousness? These are questions that families and loved-ones would very much like answers to when making decisions about ongoing care. The authors do recognize this limitation and hope to address this with future studies incorporating neurocognitive tests (9). It has been twelve years since the publication of the sentinel papers showing benefit to treating comatose survivors of cardiac arrest with mild hypothermia (1, 2). Though the adoption of the practice has been slow and not without controversy, more and more patients are treated with TTM. Previously, we may have been hesitant to render prognoses on cardiac arrest survivors that have been cooled. Now, with growing data and literature on the subject, we may finally be ready to discuss prognoses in these patients with some confidence.

Purpose. To describe a case of quadriceps tendon rupture in a patient with postanoxic choreoathetotic movements.Case report: A 20-year-old man was admitted to a rehabilitation hospital after anoxic brain injury. As a result of the injury, he developed continuous flowing choreoathetotic movements. He contracted fever and swollen and painful right knee, and only when periarticular edema decreased did a suprapatellar gap appear and quadriceps tendon rupture was diagnosed.Conclusions: Considering the possibility of tendon rupture when evaluating a patient with non-volitional movements and ‘arthritic’ presentation in a rehabilitation setting, may prevent delay of quadriceps surgical repair.

Palilalia is a rather rare speech disorder associated with a variety of etiologies including Parkinson's disease, stroke, epilepsy, and others. According to the literature, palilalia is characterized by repetitions of words, phrases, and/or sentences produced with an increasing rate and decreasing intensity. Because of the rare nature of this disorder, literature involving the characteristics is limited and somewhat contradictive. Although the original definition involves increasing rate and decreasing intensity, some researchers (i.e., Kent & Lapointe, 1982) have found different characteristics such as decreasing rate and increasing intensity when examining individual cases. This study adds to the literature regarding characteristics of palilalic speech in terms of change in rate and fundamental frequency from the original utterance to the first repeated train. This study utilized a single-subject design involving a 42 year old male who suffered an anoxic brain injury. Spontaneous speech samples were col...

A case study is presented of a 17-year-old male who sustained an anoxic brain injury and sensorineural hearing loss secondary to carbon monoxide poisoning. Audiological data is presented showing a slightly asymmetrical hearing loss of sensorineural origin and mild-to-severe degree for both ears. Word recognition performance was fair to poor bilaterally for speech presented at normal conversational levels in quiet. Management considerations of the hearing loss are discussed.

Bradycardia and transient asystole are well-described sequelae of a myriad of neurologic insults, ranging from focal to generalized injuries. Increased vagal tone also predisposes many individuals, particularly adolescents, to transient neurally mediated bradyarrhythmia. However, prolonged periods of sinus arrest without junctional or ventricular escape are quite rare, even after significant neurologic injury. We describe the case of a 17-year-old man who presented with anoxic brain injury secondary to hemorrhagic shock from a stab wound to the neck. His recovery was complicated by prolonged periods of sinus arrest and asystole, lasting over 60 seconds per episode. This case illustrates that sustained asystolic episodes may occur following significant neurologic injury, and may continue to recur even months after an initial insult. Pacemaker implantation for such patients should be strongly considered.

The outcomes of 60 children unconscious for 90 days or longer following acquired brain injury are reported. Eight children who died had remained in persistent vegetative states. As expected, most neurologic improvement occurred within the first year after injury, although some delayed improvements were observed. Outcomes were strongly correlated with causes of brain injury. Better cognitive and motor function was observed with nonanoxic injuries. No child in this report with anoxic brain injury regained functional cognitive or motor skills, although 3 became socially responsive. The remarkable contrast with adults following acquired brain injury is the significantly longer survival of children. The only children who died had remained in persistent vegetative states.

Various methods are available to induce and maintain therapeutic hypothermia after cardiac arrest, but little data is available comparing device-mediated cooling to simple surface methods in this setting.To assess the performance characteristics of simple surface cooling with or without an endovascular cooling catheter system, we retrospectively reviewed all cases of hypothermia for comatose survivors of cardiac arrest treated at a single academically affiliated urban hospital. Forty two comatose survivors of cardiac arrest were treated over a 3.5-year period. Hypothermia was induced and maintained by simple surface methods (ice packs, cooling blankets) with or without placement of an endovascular cooling catheter system with automated temperature feedback regulation.Overall, the rate of active cooling was not different between patients treated with endovascular catheter-assisted hypothermia and patients treated with surface cooling alone. However, use of a larger (14 F) catheter was associated with faster cooling rates. Maintenance of goal temperature (33 degrees C) was far better controlled with the use of a cooling catheter. Use of surface cooling alone was associated with significant temperature overshoot. Patients treated with surface cooling alone spent more time bradycardic.Use of an endovascular cooling catheter as part of a treatment protocol for hypothermia after cardiac arrest provides better control during maintenance of hypothermia, preventing temperature overshoot. Active cooling rates may be enhanced by the use of a larger cooling catheter.

Because a large number of patients will suffer cardiac arrest each year, physicians must place attention on improving care for patients in the post-resuscitative setting. Part of this effort requires setting realistic goals based on patients' potential for recovery. Recovery from cardiac arrest often depends on the extent of anoxic brain injury, and for this reason primary teams consult neurologists to offer insight into potential for awakening from post-arrest coma. In doing so, neurologists inform a decision with legal, social and ethical implications. Though inapplicable without preparation at the time of cardiac arrest, the four principles of medical ethics have a direct impact on decision making during the post-resuscitative period. A review of the literature reveals that physical examination, electrophysiology, radiology, and biochemical markers can prove useful in estimating a patient's chances for neurological recovery from cardiac arrest. These factors most reliably predict poor outcome, but do so with high specificity. However, the role of the neurology consultant must change to include guidance on strategies of neuroprotection. Aggressive efforts directed towards neuroprotection may change predictions for outcomes after cardiac arrest in the future.

Anoxic brain injury is a common outcome after cardiac arrest. Despite substantial research into the pathophysiology and management of this injury, a beneficial treatment modality has not been previously identified. Recent studies show that induced hypothermia reduces mortality and improves neurological outcomes in patients resuscitated from ventricular fibrillation. This article reviews the literature on induced hypothermia for anoxic brain injury and summarizes a treatment algorithm proposed by the Canadian Association of Emergency Physicians Critical Care Committee for hypothermia induction in cardiac arrest survivors.

Introduction. Hydrogen sulfide is a lipid-soluble gas produced in occupational settings and from decaying organic matter. We present a 36-year-old man who developed acute respiratory arrest from hydrogen sulfide poisoning while performing work as a dairy farmer. Case report. The subject entered a poorly ventilated tank containing degrading eggs and, within seconds, collapsed. Coworkers were able to extract him within minutes but he was apneic. He was intubated by emergency medical services and subsequently managed with supportive care in the intensive care unit. Upon admission, a powerful rotten egg scent was noted and a hydrogen sulfide poisoning was suspected. Serum analysis for the presence of thiosulfate confirmed the diagnosis. Nitrite therapy was not administered as the subject arrived outside of the therapeutic window of effectiveness and showed evidence of excellent oxygenation. His examinations following arrival were consistent with an anoxic brain injury which slowly improved several months after the incident with intensive neuro-rehabilitation. Discussion. Hydrogen sulfide is a mitochondrial toxin and inhibits cytochrome-aa3 and prevents cellular aerobic metabolism. Therapies for toxic exposures include removal from the contaminated environment, ventilation with 100% oxygen, and nitrite therapy if administered immediately after exposure. Hyperbaric oxygen (HBO) therapy has anecdotal support and remains controversial. Conclusion. Hydrogen sulfide is a significant occupational health hazard. Education, personal protective equipment, and early treatment are important in improving outcomes.