This chapter discusses the case of an 18-year-old woman, who had dystonia. She was sent to a psychiatric facility. She received low doses of haloperidol and a tricyclic antidepressant and after 2 weeks developed drooling, twisting of the neck to the right, and trouble walking. At that point, the psychiatrist consulted the movement disorders neurologist. She had drooling and cervical dystonia with laterocollis to the right with a mild rotational component. She presented an interesting diagnostic and treatment challenge. At the outset, the differential diagnosis consisted of primary psychiatric disorder and a possibility of drug-induced movement disorder versus a spontaneous movement disorder with psychiatric manifestations as seen in Wilson’s disease (WD). Her tests confirmed the diagnosis of WD, and she was treated with Penicillamine with the knowledge that it can cause further drop in platelets. Over the next several months, her eye movement became normal and the cervical dystonia disappeared.

This chapter discusses the case of a 38-year-old woman with diffuse, occasionally throbbing, headaches associated with nausea, which was worse while waking, together with intense pain accompanied by episodes of vomiting, diplopia, drowsiness, and torpor. Since symptoms’ onset, she reported being slower and having bilateral hand tremor. Analysis of cerebrospinal fluid (CSF) demonstrated a mild inflammatory reaction and neurocysticercosis (NCC) as detected by positive reactions to cysticercus antigens. She was assessed in the neurology service and diagnosed with intracranial hypertension after a brain MRI that showed the presence of supratentorial hydrocephalus with evidence of intraventricular cysts, as well as edema in the midbrain periaqueductal region. Methylprednisolone pulse therapy was then started, together with half a tablet of levodopa/carbidopa, with progressive improvement in the symptoms of parkinsonism. Eight months later, she was progressively taken off entacapone and then levodopa. She remained asymptomatic and returned to normal activities of daily life.

This chapter discusses the case of a 28-year-old man, who had progressive gait ataxia since the age of 16 years. Within a year, he developed dysarthria, followed by difficulties with fine finger movements. On examination, he had bilateral pes cavus and moderate scoliosis. He had gait and truncal ataxia with intention tremor, head tremor, dysmetria, dysdiadochokinesia, areflexia at lower limbs, bilateral Babinski sign, absent position and vibration senses in the feet, and positive Romberg’s sign. Neuropsychological examination revealed signs of minimal executive dysfunction. Supplementation with vitamin E in patients with ataxia with vitamin E deficiency (AVED) may improve neurologic symptoms and favorably influence prognosis. Therefore, screening for vitamin E deficiency is important in patients with ataxia of unknown etiology. Genetic analysis and early recognition of AVED may allow early introduction of effective treatment and appropriate genetic counseling.

Radiation oncologists have long understood the potential benefit of radiation therapy (RT) in palliating the distressing symptoms of advanced abdominal and pelvic cancers. Often, the role of external beam radiation therapy (EBRT) or brachytherapy in controlling bleeding or obstructive symptoms finds only a passing reference and most palliative medicine texts are silent on this important topic. Palliative RT achieves hemostasis in patients with unresectable gastric carcinoma not fit for systemic chemotherapy and is associated with a statistically significant rise in their hemoglobin levels. RT has been used for symptom relief in gynecological malignancies for many years. For abdominal malignancies, bony landmarks are less reliable for treatment planning, as compared to pelvic malignancies. This chapter discusses some case scenarios which illustrate the role of palliative radiation therapy in the treatment of bladder cancer, vaginal bleeding, rectal cancer, vulvar cancer, and liver metastasis.

Interictal epileptiform discharges (IEDs) represent a distinct group of waveforms that are characteristically seen in people with epilepsy. Scalp detection of IEDs is based upon dipole localization and the surrounding field. The interictal electroencephalogram (EEG) plays a pivotal role in providing ancillary support for a clinical diagnosis of epilepsy. Abnormal focal IEDs on EEG represent a heightened predisposition for the expression of focal seizures. Epileptiform discharges appear in different morphologies. Both spikes and sharp waves are referred to as IEDs and are defined by their duration. Mid-temporal IEDs occur in patients with temporal lobe epilepsy. Benign childhood epilepsy with centrotemporal spikes is a common childhood genetic localization related epilepsy syndrome. Frontal spikes are often found in patients with frontal lobe epilepsy, although they may be absent in up to one-third of patients. Central IEDs can occur with symptomatic focal epilepsies at any age.

Interictal electroencephalogram (EEG) provides useful information about the presence of nonepileptiform neurophysiological dysfunction. When abnormalities are encountered, they are not specific for an underlying etiology, and as such represent abnormalities without further differentiation of the pathological process. This chapter discusses and focuses on generalized and focal nonepileptiform abnormalities. Diffuse slowing on the EEG may have various morphologies, and occur intermittently or continuously, to reflect abnormal cerebral function. Low-voltage EEG is typically associated with diffuse slowing of the background rhythm. Focal abnormalities on the EEG provide electrographic evidence of a localized abnormal cerebral function. Intermittent irregular slowing has a low correlation with an underlying lesion compared to focal slowing that is continuous. EEG can reveal many types of nonepileptiform abnormalities corresponding to varied cerebral dysfunctions occurring at any age. Reactivity of nonepileptiform abnormalities is an important feature that helps assess the cause and prognosis of the clinical condition.

This chapter discusses case of a 19-year-old fine arts college student who was a very good athlete. A psychiatrist diagnosed her psychogenic gait and prescribed Clonazepam and later Seritonine reuptake inhibitors (IRSS), but no improvements were noted. She presented with dysthymia according to the DSM-III, and the movement disorder persisted unmodified. She underwent intravenous placebo therapy, but it never worked. An electromyography (EMG) was performed that did not reveal any cocontraction. The patient’s mother and sister came to the clinic and evident clinical ataxia was confirmed in both individuals with severe dysarthria and difficulties in walking without aid. She developed an increase in basal sustentation and alterations in her postural reflexes, therefore developing difficulties with walking as the disease progressed. She has almost completely recovered from the movement interpreted as “task-specific dystonia” because it has been predominantly replaced by pancerebellar ataxia with few extracerebellar signs.

The American Clinical Neurophysiology Society (ACNS) Consensus Statement on ICU continuous EEG (cEEG) provides a framework for institutions to develop cEEG monitoring programs, recognizing that this represents an "idealized" system and that many institutions do not have access to all resources described in the consensus statement. Institutions should provide cEEG at the highest level that local resources allow, with modifications as needed based on the patient's clinical status. The most common indications for ICU cEEG are: diagnosis of nonconvulsive seizures (NCS) and other paroxysmal events; assessment of efficacy of treatment of NCS; identification of cerebral ischemia; monitoring of sedation and high-dose suppressive therapy; and assessment of severity of encephalopathy and prognostication. This chapter briefly discusses clinical indications for cEEG monitoring in the ICU, qualifications of ICU EEG personnel and key aspects to implementation of an ICU EEG monitoring program.

Bone marrow failure (BMF) refers to the inability of hematopoiesis to meet the physiologic demands for the production of functional blood cells. BMF can be classified into three categories based on the presumed etiology: idiopathic, secondary, and inherited. This chapter discusses idiopathic and secondary BMF, which is usually called acquired aplastic anemia (AA). It also reviews the most common inherited bone marrow failure syndromes (IBMFSs). The clear differences in clinical management and outcomes in patients with IBMFSs compared to those with acquired AA highlight the need to have a clear understanding of these disorders and how to recognize them.