A history of the path towards imaging of the brain: From skull radiography through cerebral angiography.

This publication reviews the steps in the path towards obtaining a complete image of the brain. Up to the 1920s, plain X-ray films could demonstrate only calcified tumors, shifts in midline position of a calcified pineal gland due to a mass in the cranium, or foreign metallic objects within the skull. Walter Dandy reported in 1918 that he visualized cerebral ventricles by introducing air as a contrast agent through a trocar into one of the occipital lobes or the right frontal horn of the ventricular system. Dandy localized lesions that distorted or shifted the ventricles. In 1920, Dandy placed air by lumbar puncture into the spinal subarachnoid space that could visualize the brain and entire ventricles. Antonio Egas Moniz with the assistance of his neurosurgeon colleague, Almeida Lima, obtained X-ray images of cerebral arteries of dogs and decapitated human heads from corpses after injecting strontium bromide into their carotid arteries. Satisfied by these experiments, Moniz injected strontium bromide directly into carotid arteries of five patients which failed to show intracranial vessels. In the sixth patient, intracranial arteries were outlined but that patient died of cerebral thrombosis presumably due to the hyper-osmolality of that contrast agent. Finally, on June 18, 1927, Moniz injected 22% sodium iodine into a 20-year-old man and obtained clear visualization of his carotid artery and intracerebral branches after temporarily occluding the artery with a ligature. Direct percutaneous puncture of the cervical carotid artery remained the primary technique unto the 1960s to visualize intracranial blood vessels until Seldinger's technique was introduced in 1953. Computerized axial tomography (CAT) and magnetic resonance imaging (MRI) replaced cerebral arteriography for localizing tumors and epidural or subdural hemorrhage. However, angiography is used currently for embolization of aneurysms and removal of thrombi or emboli in patients with acute stroke.

Alice in Wonderland Syndrome: A Historical and Medical Review.

Alice in Wonderland syndrome is a disorienting neurological condition that affects human perception to the senses of vision, hearing, touch, sensation, and the phenomenon of time. Individuals affected with Alice in Wonderland syndrome can experience alterations in their perception of the size of objects or their own body parts, known as metamorphopsias. It is known to occur in conditions including migraine, epilepsy, and certain intoxicants and infectious diseases. The name refers to Lewis Carrol's well-known children's book Alice's Adventures in Wonderland, in which the title character experiences alterations of sensation in which she felt that her body had grown too tall or too small, or parts of her body were changing shape, size, or relationship to the rest of her body. The syndrome was described in 1952 by Caro Lippman, and given its name in 1955 by John Todd. The metamorphopsias characteristic of this condition are also sometimes referred to as Lilliputian hallucinations, a reference to the fictional island of Lilliput in the novel Gulliver's Travels, written by Jonathan Swift in 1726. As such, many literary and medical publications have roots in the description of this syndrome. The purpose of this review is to summarize the literary and historical significance of Alice in Wonderland syndrome, as well as to provide the reader with a medical overview of the condition.

What's in the Literature?

In this edition of this column, we review new studies concerning the pathophysiology, treatment, and outcomes of patients with necrotizing myopathy, genetic testing in congenital myopathies, and limb girdle muscular dystrophies, and the incidence of polyneuropathy in the myotonic dystrophies. Various studies in myasthenia gravis, including those concerning antibody testing, clinical features, and quality of life are also reviewed as are recent findings in congenital myasthenic syndromes. Finally, 2 studies concerning polyneuropathy are discussed, including one on the association of polyneuropathy in patients with the metabolic syndrome and one on laboratory testing in patients with otherwise idiopathic small fiber polyneuropathy.

Disappearance of thalamic pain after parietal subcortical stroke.

A hypertensive man had a long standing history of contumacious hyperpathia in the right upper extremity, resistant to medical therapy, secondary to a lacunar infarct in the left thalamus. A second cerebrovascular accident caused a small lesion in the left corona radiata, interrupting the thalamoparietal interconnections, and terminated the pain instantly. Interruption of the subcortical parietal white matter may more effectively control pain than cortical lesions. A few surgeons have successfully treated rebellious chronic pain with stereotaxic operations in the corona radiata, resulting in lesions very similar to our patient's. This overlooked and nearly forgotten technique may still have value in treating selected cases.

The Alice in Wonderland syndrome.

The Alice in Wonderland syndrome is a term applied to altered bizarre perceptions of size and shapes of a patient's body and illusions of changes in the forms, dimensions, and motions of objects that a patient with this syndrome encounters. These metamorphopsias arise during complex partial seizures, migraine headaches, infections, and intoxications. The illusions and hallucinations resemble the strange phenomena that Alice experienced in Lewis Carroll's Alice's Adventures in Wonderland. Charles Lutwidge Dodgson, whose nom de plume was Lewis Carroll, experienced metamorphopsias. He described them in the story that he wrote for Alice Liddell and her two sisters after he spun a tale about a long and strange dream that the fictional Alice had on a warm summer day. The author of this chapter suggests that Dodgson suffered from migraine headaches and used these experiences to weave an amusing tale for Alice Liddell. The chapter also discusses the neurology of mercury poisoning affecting the behavior of Mad Hatter character. The author suggests that the ever-somnolent Dormouse suffered from excessive daytime sleepiness due to obstructive sleep apnea.

Neurognostics question. Gordon Morgan Holmes.

Gordon Morgan Holmes, MD, MRCP was an Irish born neurologist who received his medical education at Trinity College, Dublin, Ireland. He was trained in neuroanatomy and neuropathology at the Senckenberg Institute, Frankfort-Am-Main by Ludwig Edinger. He then returned to serve as a Registrar (House Officer) mentored by Richard Gowers and John Hughlings Jackson at the National Hospital, Queen Square, London. He collaborated with Thomas Granger Stewart in describing the loss of recoil in patients with cerebellar hemispheric tumors in 1904. Volunteering in 1914 for frontline hospital duty, he examined soldiers who had injuries to their occipital area causing hypotonia, dysmetria, staggering gait, and falling to the side ipsilateral to their injured cerebellar hemisphere. Holmes discovered that increasing the pace of the finger-nose manuever and applying slight resistance to a moving limb attenuated the dysmetria. Continuing observation of these patients afforded him to describe the evolution of their injuries to include increasing tremor and decreasing hypotonia. Holmes first attached levers to the limbs of hispatients to record their movements on a moving smoked paper kymograph. In 1939 he published photograh tracings made by low mass minature light bulbs attached to ataxic limbs that showed thehpometira and hypometria of their movements ipsilateral to their damaged cerebellar lobes. Holmes made sigficant contributions to understanding of the physiology of the human cerebellum.

The history of the development of the cerebellar examination.

The cerebellar examination evolved from observations of experimental lesions made by neurophysiologists and clinical descriptions of patients with trauma to the cerebellum. At the beginning of the 19th century, neurophysiologists such as Luigi Rolando, Marie-Jean-Pierre Flourens, and John Call Dalton, Jr. ablated portions of the cerebellum of a variety of animals and observed staggering gait, clumsiness, and falling from side to side without loss of strength. They concluded that the cerebellum coordinated voluntary movements. In 1899, Joseph Francois Félix Babinski observed that patients with cerebellar lesions could not execute complex movements without breaking down into their elemental movements and described the defect as dysmetria. In 1902, Babinski coined the term dysdiodochokinesis to describe the inability to perform rapid execution of movements requiring alternate contractions of agonist and antagonist muscles. Gordon Holmes in 1904 described the phenomena of rebound, noting that if a limb ipsilateral to a cerebellar lesion is suddenly released from tension, the appendage will flail. In 1917, Gordon Holmes reported hypotonia and dysmetria in men wounded by gunshot wounds to their cerebellum. These observations were rapidly included in descriptions of the cerebellar examination in popular contemporaneous textbooks of neurology. Modern observations have demonstrated that the cerebellum influences such cognitive functions such as planning, verbal fluency, abstract reasoning, prosody, and use of correct grammar.