Fisiología Linda S.

Costanzo
Visit to download the full and correct content document:
https://ebookmass.com/product/fisiologia-linda-s-costanzo/
Fisiología

SEXTA EDICIÓN

Linda S. Costanzo, PhD

Professor of Physiology and Biophysics
Virginia Commonwealth University School of Medicine
Richmond, Virginia

******ebook converter DEMO Watermarks*******

Índice de capítulos

Instrucciones para el acceso en línea

Cubierta

Portada

Página de créditos

Dedicatoria

Prefacio

Agradecimientos

Capítulo 1: Fisiología celular

Volumen y composición de los líquidos corporales

Características de las membranas celulares

Transporte a través de las membranas celulares

Potenciales de difusión y de equilibrio

Potencial de membrana en reposo

******ebook converter DEMO Watermarks*******

 Potenciales de acción

Transmisión sináptica y neuromuscular

Músculo esquelético

Músculo liso

Resumen

Capítulo 2: Sistema nervioso autónomo

Organización y características generales del sistema nervioso autónomo

Receptores autónomos

Resumen

Capítulo 3: Neurofisiología
Organización del sistema nervioso

Células del sistema nervioso

Características generales de los sistemas sensorial y motor

Sistemas sensoriales

Sistema somatosensorial y dolor

Visión

Audición

Sistema vestibular

Olfato

Gusto

Sistemas motores

Funciones superiores del sistema nervioso

Líquido cefalorraquídeo

Resumen

******ebook converter DEMO Watermarks*******

Capítulo 4: Fisiología cardiovascular
Circuito del sistema cardiovascular

Hemodinámica

Electrofisiología cardíaca

Contracción del músculo cardíaco

Ciclo cardíaco

Relaciones entre el gasto cardíaco y el retorno venoso

Regulación de la presión arterial

Microcirculación

Circulaciones especiales

Termorregulación

Funciones integradoras del sistema cardiovascular

Resumen

Capítulo 5: Fisiología respiratoria

Estructura del sistema respiratorio

Volúmenes y capacidades pulmonares

Mecánica de la respiración

Intercambio de gases

Transporte de oxígeno en la sangre

Transporte de dióxido de carbono en la sangre

Relaciones ventilación/perfusión

Control de la respiración

Funciones integradoras

Hipoxemia e hipoxia

Resumen

******ebook converter DEMO Watermarks*******

Capítulo 6: Fisiología renal
Anatomía y aporte sanguíneo

Líquidos corporales

Aclaramiento renal

Flujo sanguíneo renal

Filtración glomerular

Reabsorción y secreción

Terminología asociada a la nefrona

Equilibrio del sodio

Equilibrio del potasio

Equilibrio del fosfato, el calcio y el magnesio

Equilibrio hídrico: concentración y dilución de orina

Resumen

Capítulo 7: Fisiología acidobásica

pH de los líquidos corporales

Producción de ácido en el organismo

Neutralización

Mecanismos renales en el equilibrio acidobásico

Trastornos del equilibrio acidobásico

Resumen

Capítulo 8: Fisiología gastrointestinal

Estructura del aparato digestivo

Inervación del aparato digestivo

Sustancias reguladoras gastrointestinales

******ebook converter DEMO Watermarks*******

 Motilidad

Secreción

Digestión y absorción

Transporte hidroelectrolítico intestinal

Fisiología del hígado

Resumen

Capítulo 9: Fisiología endocrina

Síntesis hormonal

Regulación de la secreción hormonal

Regulación de los receptores hormonales

Mecanismos de acción hormonal y segundos mensajeros

Relaciones hipotalámico-hipofisarias

Hormonas del lóbulo anterior de la hipófisis

Hormonas del lóbulo posterior de la hipófisis

Hormonas tiroideas

Médula y corteza suprarrenales

Páncreas endocrino

Regulación del metabolismo del calcio y del fosfato

Resumen

Capítulo 10: Fisiología reproductiva

Diferenciación sexual

Pubertad

Fisiología reproductiva masculina

Fisiología reproductiva femenina

******ebook converter DEMO Watermarks*******

 Resumen

Apéndice I: Abreviaturas y símbolos frecuentes

Apéndice II: Constantes y valores normales

Respuestas a los cuestionarios de autoevaluación

Índice alfabético

******ebook converter DEMO Watermarks*******

Página de créditos

Avda. Josep Tarradellas, 20-30, 1.°, 08029, Barcelona, España

Physiology
© 2018 by Elsevier, Inc. All rights reserved

Previous editions copyrighted 2014, 2010, 2006, 2002, 1998

ISBN: 978-0-323-47881-6

This translation of Physiology, 6e., by Linda S. Costanzo, was

undertaken by Elsevier España, S.L.U. and is published by
arrangement with Elsevier, Inc.

Esta traducción de Physiology, 6.ª ed., de Linda S. Costanzo, ha sido

llevada a cabo por Elsevier España, S.L.U. y se publica con el permiso
de Elsevier, Inc.

Fisiología, 6.ª ed., de Linda S. Costanzo

© 2018 Elsevier España, S.L.U.

ISBN: 978-84-9113-273-8
eISBN: 978-84-9113-333-9

Todos los derechos reservados.

Reserva de derechos de libros

Cualquier forma de reproducción, distribución, comunicación pública
o transformación de esta obra solo puede ser realizada con la
******ebook converter DEMO Watermarks*******
autorización de sus titulares, salvo excepción prevista por la ley.
Diríjase a CEDRO (Centro Español de Derechos Reprográficos) si
necesita fotocopiar o escanear algún fragmento de esta obra
(www.conlicencia.com; 91 702 19 70 / 93 272 04 45).

Advertencia
Esta traducción ha sido llevada a cabo por Elsevier España, S.L.U. bajo
su única responsabilidad. Facultativos e investigadores deben siempre
contrastar con su propia experiencia y conocimientos el uso de
cualquier información, método, compuesto o experimento descrito
aquí. Los rápidos avances en medicina requieren que los diagnósticos
y las dosis de fármacos recomendadas sean siempre verificadas
personalmente por el facultativo. Con todo el alcance de la ley, ni
Elsevier, ni los autores, los editores o los colaboradores asumen
responsabilidad alguna por la traducción ni por los daños que
pudieran ocasionarse a personas o propiedades por el uso de
productos defectuosos o negligencia, o como consecuencia de la
aplicación de métodos, productos, instrucciones o ideas contenidas en
esta obra.

Revisión científica:
Xavier Gasull Casanova
Profesor titular de Fisiología
Facultad de Medicina. Universidad de Barcelona

Servicios editoriales: DRK Edición

Depósito legal: B 1185-2018

Impreso en Barcelona

******ebook converter DEMO Watermarks*******

Dedicatoria

Heinz Valtin y Arthur C. Guyton,

que tan bien han escrito para los estudiantes de Fisiología

Richard, Dan, Rebecca, Sheila, Elise y Max,

que hacen que todo merezca la pena

******ebook converter DEMO Watermarks*******

Prefacio
La fisiología es la base de la práctica médica. Es fundamental que el
estudiante de medicina y el médico en ejercicio posean unos sólidos
conocimientos de sus principios. Este libro se dirige a estudiantes de
Medicina y de otras disciplinas de ciencias de la salud que estudian la
fisiología. Puede utilizarse como material complementario de las
clases o como fuente principal de aprendizaje en la enseñanza
integrada o basada en problemas. Para estudiantes avanzados, el libro
puede servir de referencia en cursos de fisiopatología y en rotaciones
clínicas.
En la sexta edición de esta obra, igual que en ediciones anteriores, se
tratan los conceptos importantes de la fisiología tanto a nivel de
sistemas como celular. En los capítulos 1 y 2, se presentan los
principios básicos de la fisiología celular y del sistema nervioso
autónomo. Los capítulos 3 a 10 presentan los principales sistemas
orgánicos: neurofisiología y fisiología cardiovascular, respiratoria,
renal, acidobásica, gastrointestinal, endocrina y reproductiva. Se ha
hecho hincapié en las relaciones entre los diferentes sistemas
orgánicos para destacar los mecanismos integradores de la
homeostasis.
Esta edición incluye las siguientes características diseñadas para
facilitar el estudio de la fisiología:

♦ Texto conciso y de fácil lectura: las diversas categorías de los

títulos guían al estudiante en la comprensión de la estructura
jerárquica de los contenidos. La información fisiológica
compleja se presenta de manera sistemática, lógica y gradual.
Cuando un proceso tiene lugar siguiendo una secuencia
específica, los pasos se numeran en el texto y con frecuencia se
******ebook converter DEMO Watermarks*******
 correlacionan con los números mostrados en la figura
correspondiente. Las viñetas se utilizan para separar y resaltar
las características de un proceso. A lo largo del texto se
plantean preguntas retóricas para anticiparse a las que
podrían plantearse los estudiantes; al pensar y posteriormente
responder a estas preguntas, los estudiantes aprenden a
explicar conceptos difíciles y racionalizar hallazgos
imprevistos o paradójicos. Los resúmenes de los capítulos
ofrecen una breve perspectiva general.
♦ Tablas e ilustraciones que pueden utilizarse junto con el texto
o de forma individual como repaso, ya que han sido diseñadas
de forma independiente al texto : las tablas resumen, ordenan
y hacen comparaciones. Algunos ejemplos de este tipo de
tablas son: 1) una tabla que compara las hormonas
gastrointestinales con respecto a la familia de hormonas, el
lugar y los estímulos de secreción y sus diferentes acciones, 2)
una tabla que compara las características fisiopatológicas de
los trastornos de la homeostasis del Ca2+ y 3) una tabla que
compara las características del potencial de acción en
diferentes tejidos cardíacos. Las ilustraciones están claramente
diferenciadas, a menudo con títulos principales, e incluyen
diagramas simples, diagramas complejos con pasos
numerados y diagramas de flujo.
♦ Ecuaciones y problemas de ejemplo integrados en el texto: se
definen todos los términos y unidades de las ecuaciones y
cada ecuación se replantea en palabras para situarla en un
contexto fisiológico. Los problemas van seguidos de
soluciones numéricas y explicaciones completas que guían a
los estudiantes paso a paso por el razonamiento correcto. Así,
los estudiantes adquieren las habilidades y la confianza para
resolver problemas similares o relacionados.
♦ Fisiología clínica presentada en cuadros: cada cuadro explica
el caso de un paciente ficticio con un trastorno clásico. Los
hallazgos clínicos y el tratamiento propuesto se explican
basándose en los principios fisiológicos subyacentes. Se

******ebook converter DEMO Watermarks*******

 realiza un abordaje integrado para subrayar las relaciones
entre los diferentes sistemas de órganos. Por ejemplo, el caso
de diabetes mellitus tipo 1 no sólo incluye un trastorno del
sistema endocrino, sino también de los sistemas renal, acido-
básico, respiratorio y cardiovascular.
♦ Preguntas prácticas en las secciones de «Autoevaluación» al
final de cada capítulo: las preguntas prácticas, formuladas
para respuestas cortas (una palabra, una frase o una solución
numérica) obligan al estudiante a aplicar principios y
conceptos en la resolución de problemas, en vez de recordar
hechos aislados. Las preguntas se plantean en varios formatos
y están ordenadas de forma aleatoria. Serán más útiles cuando
se utilicen como herramienta después de estudiar cada
capítulo y sin consultar el texto. De esta manera, el estudiante
puede confirmar su conocimiento de la asignatura y
determinar qué áreas debe repasar. Las respuestas se
encuentran al final del libro.
♦ Vídeos sobre temas seleccionados: dado que en ocasiones son
oportunas las explicaciones orales de ciertos principios
complejos, se incluyen una serie de breves vídeos educativos
que complementan el texto escrito.
♦ Abreviaturas y valores normales que se presentan en dos
apéndices al final de libro. A medida que los estudiantes
consulten y utilicen esta información, irán familiarizándose
con ella.

Este libro plasma tres ideas que tengo sobre la docencia: 1) incluso
la información compleja puede transmitirse claramente si se presenta
de manera sistemática, lógica y gradual; 2) la presentación puede ser
tan eficaz impresa como en persona, y 3) los estudiantes de medicina
de los primeros cursos desean materiales docentes que sean precisos y
didácticamente sólidos, pero sin los detalles que ante todo interesan a
los expertos. Esencialmente, un libro puede «enseñar» si la voz del
profesor está presente, si el material es seleccionado cuidadosamente
para incluir información básica y si se presta una gran atención a la

******ebook converter DEMO Watermarks*******

lógica y a la secuencia. Este texto ofrece una presentación profesional
y pragmática dedicada a y para los estudiantes.
Espero que los lectores de este libro disfruten del estudio de la
fisiología. Quienes aprendan bien sus fundamentos recibirán su
recompensa durante sus carreras profesionales.
Linda S. Costanzo

******ebook converter DEMO Watermarks*******

Agradecimientos
Quiero agradecer las contribuciones de Elyse O’Grady, Jennifer Ehlers
y Dan Fitzgerald, de Elsevier, en la preparación de la sexta edición de
Fisiología. El ilustrador, Matthew Chansky, revisó las figuras existentes
y creó otras nuevas, y todas ellas complementan el texto a la
perfección.
Mis colegas de la Virginia Commonwealth University han
respondido fielmente a mis preguntas, especialmente los Dres. Clive
Baumgarten, Diomedes Logothetis, Roland Pittman y Raphael
Witorsch. También deseo expresar mi más sincero agradecimiento a
los estudiantes de Medicina de todo el mundo que generosamente han
compartido conmigo sus experiencias con las ediciones previas del
libro.
Mi marido, Richard, nuestros hijos, Dan y Rebecca, nuestra nuera
Sheila y nuestros nietos Elise y Max, han ofrecido un apoyo entusiasta
y un amor incondicional, que dan al libro su esencia.

******ebook converter DEMO Watermarks*******

CAPÍTULO 1

******ebook converter DEMO Watermarks*******

Fisiología celular

Volumen y composición de los líquidos corporales

Características de las membranas celulares
Transporte a través de las membranas celulares
Potenciales de difusión y de equilibrio
Potencial de membrana en reposo
Potenciales de acción
Transmisión sináptica y neuromuscular
Músculo esquelético
Músculo liso
Resumen
Autoevaluación

Entender las funciones de los sistemas orgánicos requiere un

profundo conocimiento de los mecanismos celulares básicos. Aunque
cada sistema orgánico tiene una función global diferente, todos parten
de un conjunto común de principios fisiológicos.
En este capítulo se presentan los siguientes principios básicos de
fisiología: los líquidos corporales, con especial hincapié en las
diferencias de composición del líquido intracelular y extracelular; la
creación de estas diferencias de concentración por procesos de
transporte en las membranas celulares; el origen de la diferencia de
potencial eléctrico a través de las membranas celulares, especialmente
******ebook converter DEMO Watermarks*******
en células excitables como las del nervio y el músculo; la generación
de potenciales de acción y su propagación en células excitables; la
transmisión de información entre células a través de las sinapsis y el
cometido de los neurotransmisores, y los mecanismos que conectan
los potenciales de acción a la contracción en las células musculares.
Estos principios de fisiología celular forman un grupo de temas
recurrentes e interrelacionados que, una vez comprendidos, pueden
aplicarse e integrarse en la función de cada sistema orgánico.

******ebook converter DEMO Watermarks*******

Volumen y composición de los líquidos
corporales
Distribución del agua en los
compartimentos de líquidos corporales
El agua constituye una proporción considerable del peso del cuerpo
humano. La cantidad total de líquido o agua se llama agua corporal
total y representa del 50% al 70% del peso corporal. Por ejemplo, un
hombre de 70 kilos (kg), cuya agua corporal total representa el 65% de
su peso, tiene 45,5 kg o 45,5 litros (l) de agua (1 kg de agua ≈1 l de
agua). En general, el agua corporal total es inversamente proporcional
a la grasa corporal. Por tanto, el agua corporal total representa un
porcentaje mayor del peso cuando la grasa corporal es baja, y un
porcentaje menor cuando la grasa corporal es alta. Dado que las
mujeres tienen un porcentaje mayor de tejido adiposo que los
hombres, tienden a contener menos agua corporal. La distribución del
agua en los compartimentos de los líquidos corporales se describe
brevemente en este capítulo y con mayor detalle en el capítulo 6.
El agua corporal total se distribuye en dos grandes compartimentos
de líquidos corporales: el líquido intracelular (LIC) y el líquido
extracelular (LEC) (fig. 1.1). El LIC está en el interior de las células y
constituye dos terceras partes del agua corporal total; el LEC está en el
exterior de las mismas y supone una tercera parte del agua corporal
total. El LIC y el LEC están separados por las membranas celulares.

******ebook converter DEMO Watermarks*******

 FIG. 1.1 Compartimentos de los líquidos corporales.

El LEC se divide, a su vez, en dos compartimentos: el plasma y el

líquido intersticial. El plasma es el líquido que circula por los vasos
sanguíneos y es el más pequeño de los dos subcompartimentos del
LEC. El líquido intersticial es el líquido que realmente baña las
células y el mayor de los dos subcompartimentos. El plasma y el
líquido intersticial están separados por la pared capilar, y este
segundo es un ultrafiltrado del plasma formado mediante procesos
de filtración a través de la pared capilar. Puesto que la pared capilar es
prácticamente impermeable a moléculas grandes como las proteínas
del plasma, el líquido intersticial contiene pocas proteínas o ninguna.
En el capítulo 6 se presenta el método para calcular el volumen de
los compartimentos de líquidos corporales.

Composición de los compartimentos de

líquidos corporales
La composición de los líquidos corporales no es uniforme. El LIC y el
LEC tienen concentraciones muy diferentes de diversos solutos.
También existen algunas diferencias predecibles en las

******ebook converter DEMO Watermarks*******

concentraciones de solutos entre el plasma y el líquido intersticial que
son consecuencia de la exclusión de proteínas del líquido intersticial.

Unidades para medir las concentraciones de solutos

Habitualmente, las cantidades de soluto se expresan en moles,
equivalentes u osmoles. Asimismo, las concentraciones de solutos se
expresan en moles por litro (mol/l), equivalentes por litro (Eq/l) u
osmoles por litro (Osm/l). En las soluciones biológicas, las
concentraciones de solutos suelen ser bastante bajas y se expresan en
milimoles por litro (mmol/l), miliequivalentes por litro (mEq/l) o
miliosmoles por litro (mOsm/l).
Un mol son 6 × 1023 moléculas de una sustancia. Un milimol son
1/1.000 o 10−3 moles. Una concentración de glucosa de 1 mmol/l tiene
1 × 10−3 moles de glucosa en 1 l de solución.
Se usa un equivalente para describir la cantidad de soluto cargado
(ionizado), y es el número de moles del soluto multiplicado por su
valencia. Por ejemplo, un mol de cloruro potásico (KCl) en solución se
disocia en un equivalente de potasio (K+) y un equivalente de cloro
(Cl–). Asimismo, un mol de cloruro cálcico (CaCl2) en solución se
disocia en dos equivalentes de calcio (Ca2+) y dos equivalentes de cloro
(Cl−); por consiguiente, una concentración de Ca2+ de 1 mmol/l
equivale a 2 mEq/l.
Un osmol es el número de partículas en las que se disocia un soluto
en solución. La osmolaridad es la concentración de partículas en
solución expresada en osmoles por litro. Si un soluto no se disocia en
solución (p. ej., glucosa), entonces su osmolaridad es igual a su
molaridad. Si un soluto se disocia en más de una partícula en solución
(p. ej., NaCl), entonces su osmolaridad es igual a la molaridad
multiplicada por el número de partículas en solución. Por ejemplo,
una solución que contiene 1 mmol/l de NaCl es 2 mOsm/l, porque el
NaCl se disocia en dos partículas.
El pH es un término logarítmico que se utiliza para expresar la
concentración de hidrógeno (H+). Debido a que la concentración de H+
de los líquidos corporales es muy baja (p. ej., 40 × 10−9 Eq/l en sangre
arterial), se expresa de forma más práctica como un término

******ebook converter DEMO Watermarks*******

logarítmico, el pH. El signo negativo significa que el pH disminuye a
medida que aumenta la concentración de H+, y el pH aumenta a
medida que disminuye la concentración de H+. Por tanto,

Problema
Dos hombres, el sujeto A y el sujeto B, tienen trastornos que causan
una producción excesiva de ácido en el organismo. Los análisis
indican la acidez de la sangre del sujeto A en términos de [H+] y la
acidez de la sangre del sujeto B en términos de pH. El sujeto A tiene
una [H+] arterial de 65 × 10–9 Eq/l, y el B tiene un pH arterial de 7,3.
¿Cuál de ellos tiene la mayor concentración de H+ en la sangre?
Solución
Para comparar la acidez de la sangre de cada sujeto, convierta la [H+]
del sujeto A a pH de la siguiente forma:

******ebook converter DEMO Watermarks*******

 Por tanto, el sujeto A tiene un pH sanguíneo de 7,19 calculado a
partir de la [H+], y el B, de 7,3. El sujeto A tiene un pH sanguíneo más
bajo, lo que refleja una mayor [H+] y un estado más ácido.

Electroneutralidad de los compartimentos de líquidos

corporales
Cada compartimento de líquidos corporales debe obedecer al
principio de electroneutralidad macroscópica; es decir, cada
compartimento debe tener la misma concentración, en mEq/l, de
cargas positivas (cationes) y de cargas negativas (aniones). No puede
haber más cationes que aniones, y viceversa. Incluso cuando existe
una diferencia de potencial a través de la membrana celular, el
equilibrio de las cargas aún se mantiene en las soluciones globales
(macroscópicas). Debido a que las diferencias de potencial se crean
por la separación de solo unas pocas cargas adyacentes a la
membrana, esta pequeña separación de cargas no es suficiente para
cambiar perceptiblemente las concentraciones globales.

Composición de los líquidos intracelular y extracelular

******ebook converter DEMO Watermarks*******

Las composiciones del LIC y del LEC son notablemente diferentes,
como se muestra en la tabla 1.1. El principal catión del LEC es el sodio
(Na+) y los aniones de equilibrio son cloro (Cl−) y bicarbonato (HCO3−).
Los principales cationes del LIC son potasio (K+) y magnesio (Mg2+), y
los aniones de equilibrio son proteínas y fosfatos orgánicos. Otras
diferencias significativas de composición afectan al Ca2+ y al pH.
Habitualmente, el LIC tiene una concentración muy baja de Ca2+
ionizado (≈10−7 mol/l), mientras que la concentración de Ca2+ en el LEC
es mayor, de aproximadamente cuatro órdenes de magnitud. El LIC es
más ácido (tiene un pH más bajo) que el LEC. Por tanto, las sustancias
que se encuentran en concentraciones altas en el LEC tienen
concentraciones bajas en el LIC, y viceversa.

Tabla 1.1
Composiciones aproximadas de los líquidos intracelular y extracelular

Sustancia y unidades Líquido extracelular Líquido intracelulara

Na+ (mEq/l) 140 14
K+ (mEq/l) 4 120
Ca2+, ionizado (mEq/l) 2,5b 1 × 10–4
Cl− (mEq/l) 105 10
HCO3− (mEq/l) 24 10
pHc 7,4 7,1
Osmolaridad (mOsm/l) 290 290
a
Los principales aniones del líquido intracelular son proteínas y fosfatos orgánicos.
b
El [Ca2+] total correspondiente en el líquido extracelular es de 5 mEq/l o 10 mg/dl.
c
El pH es −log10 de la [H+]; un pH de 7,4 corresponde a una [H+] de 40 × 10−9 Eq/l.

Sorprendentemente, dadas las diferencias de concentración de

solutos individuales, la concentración total de solutos (osmolaridad)
es igual en el LIC y el LEC. Esta equivalencia se consigue porque el
agua fluye libremente a través de las membranas celulares. Cualquier
diferencia transitoria de la osmolaridad que haya entre el LIC y el LEC
se disipa rápidamente por el movimiento del agua hacia el interior o
el exterior de las células para restablecer la equivalencia.

Creación de diferencias de concentración a través de las

membranas celulares

******ebook converter DEMO Watermarks*******

Another random document with
no related content on Scribd:
cases collected by Mouchet, 3 ended in recovery. Another success
has been recently recorded by Turretta. The écraseur has been
used, but its employment cannot be recommended. Compression by
clamps is advised by Schatz of Rostock. Ligation is best adapted to
cases occurring in the cervical and dorsal regions, in which, as
pointed out by Giraldès, nerve-elements are less likely to be
involved. Excision, supplemented by transplantation of a strip of
periosteum from a rabbit, has been successfully resorted to by
Mayo-Robson and by R. T. Hayes of Rochester, N. Y.; and simple
excision, with suture in separate lines of the sac and integuments, by
Mayo-Robson, Atkinson, and Jessop. The Clinical Society's
committee in all refers to 23 cases treated by excision, 16 of which
are said to have been successful.

ANÆMIA AND HYPERÆMIA OF THE BRAIN AND

SPINAL CORD.

BY E. C. SPITZKA, M.D.

Cerebral Hyperæmia.
Up to within a few years it was a favorite mode of explaining the
results of the administration of certain narcotic and stimulant drugs,
and certain of the active symptoms of mental derangement, to
attribute them to an increased blood-supply of the nerve-centres.
This view seemed to harmonize so thoroughly with the physiological
dictum that functional activity depends on the supply of oxygenated
blood that the first attempts at questioning it were treated as
heresies. To-day, however, few authorities can be found to adhere
unreservedly to this once-popular and easy explanation. The drift of
physiological and medical opinion is in the direction of regarding
some subtle molecular and dynamic state of the nerve-elements as
the essential factor in intoxications as well as in maniacal and other
forms of insane excitement: if they be complicated by active or
passive congestions, this is probably a secondary occurrence of
modifying but not of intrinsic determining power. While this change in
our views is the natural result of progress in experimental
pharmacology and pathology, it does not justify the extreme
assertion that there is no disorder of the brain functions deserving
the name of congestion and hyperæmia. This assertion seems to
have been provoked by the careless manner in which these terms
have been employed to designate conditions which are in reality the
most different in nature that can be well conceived. No one familiar
with the extent to which the term “congestion of the base of the
brain” has been abused in this country will marvel that the reaction
provoked by it has overstepped the boundaries of cautious criticism.
That there are physiological hyperæmias of the brain is now
universally admitted; the most recent experimental observations,
indeed, conform most closely to the claims of the older investigators.
It naturally follows that pathological hyperæmias are both possible
and probable, and even if the observations in the dead-house do not
strongly sustain the existence of pathological hyperæmias and
congestions independently of gross disease, clinical analysis and the
gratifying results of appropriate treatment justify us in retaining these
designations in our nomenclature with the limitation here implied.

One great difficulty in determining the precise nature of the disorders

which the physician is called upon to treat on the theory of
hyperæmia lies in the number of factors which may contribute to or
modify its development. If, for example, the action of the heart be
increased through hypertrophy, the result to the cerebral circulation
will obviously be different in a plethoric and in an anæmic person; it
will be also very much different in the event of the stimulation of the
centres which contract the calibre of the cerebral blood-vessels from
what it would be if there were a state of vascular relaxation. Should
the cardiac hypertrophy be associated with renal disease, other
disturbing elements may be introduced, such as arterio-fibrosis, or
the presence in the blood of certain toxic substances having direct
effects of their own on the nerve-elements. The picture may be still
more complicated by variations in the intracranial pressure. It is
impossible to prove, either by direct or indirect evidence, that there is
such a pathological state as a simple cerebral hyperæmia; indeed,
there is one fact which militates strongly against, if it be not fatal to,
such an assumption. Were a physiological hyperæmia to become
intensified to a pathological degree, we should have corresponding
clinical phenomena. In other words, the culmination of the morbid
process should be preceded by an exaggerated physiological
excitation similar to that observed with intoxications. But this is rarely
the case, and we accordingly find that the more cautious writers, like
Nothnagel,1 do not commit themselves to the view that the results of
mental overstrain2 are to be classed as simple cerebral hyperæmia.
Similar restrictions are to be made regarding the established
congestive states, such as those following sunstroke. It has been
usually supposed that insolation directly produces cerebral
hyperæmia, even to the degree of engorgement, and that the after
symptoms in persons who recover are due to the non-return of the
meningeal and cerebral blood-vessels to their normal calibre, and to
other more remote results of vascular stasis. The latter half of this
proposition is in part correct; the former is contradicted by numerous
pathological observations. Thus, Arndt,3 who had the opportunity of
studying over one hundred cases occurring in the course of a forced
march of a division of infantry from Berlin to Pankow, many of which
terminated fatally, found almost uniformly a pale brain, with peculiar
color-changes, denoting rather structural than circulatory trouble.4
The whole list of causes of what is commonly designated cerebral
hyperæmia, congestion, and engorgement may be gone through
with and similar modifying statements be found to apply to them. The
nearest approach to an ideal cerebral congestion is that found with
acute alcoholic intoxication. This is at first accompanied by cerebral
hyperæmia, which, with the comatose climax, becomes an
engorgement; accordingly, many of the results of acute alcoholic
intoxication are attributed to the circulatory condition alone. The
congestive troubles due to alcoholism which come to the special ken
of the physician, however, are those found with the chronic form, and
here a more complex pathological condition is found to underlie it;
the organization of the brain is altered, the vascular channels more
or less diseased, and the vaso-motor mechanism continuously
deranged. This disorder, as well as the apoplectiform states
attributed to vascular stasis, and the active and passive hyperæmias
associated with tumors, meningitic and other gross diseases of the
brain, as well as with the status epilepticus, are usually included in
the discussion of cerebral congestion, and serve to swell up the
chapters devoted to it. They will be found discussed in more
appropriate situations in this volume. In this place it is proposed to
consider only those congestive states which present themselves to
the physician, independently of conditions which, if associated,
preponderate in clinical and therapeutic importance.5
1 Ziemssen's Cyclopædia, “Nervous System,” i. p. 39, 2d German ed.

2 It has repeatedly happened during the past decade that young persons competing
for admission to higher institutions of learning in New York City through the channel of
a competitive examination died with symptoms of cerebral irritation; the death
certificates in several such cases assigned meningitis or cerebral congestion as the
cause of death, and attributed the disorder to mental overstrain. It is not so much the
intellectual effort that has proved hurtful to the pupils as the emotional excitement
attending on all competitive work, the dread of failure, the fear of humiliation, and
anxiety developed by the evident futility of the cramming process. Some years ago I
recorded the results of some inquiries on this head in the following words: “The
mental-hygiene sensationalists, who periodically enlighten the public through the
columns of the press whenever an opportune moment for a crusade against our
schools and colleges seems to have arrived, are evidently unaware of the existence
 of such a disease as delirium grave, and ignorant of the fact that the disorder which
they attribute to excessive study is in truth due to a generally vitiated mental and
physical state, perhaps inherited from a feeble ancestry. Our school system is
responsible for a good deal of mischief, but not for meningitis” (Insanity, its
Classification, Diagnosis, and Treatment). Since then I had an opportunity of obtaining
an excellent description of such a case which had been attributed to the combined
effects of malaria and educational overstrain, presenting opisthotonos, fulminating
onset, and an eruption!

3 Virchow's Archiv, lxiv.

4 The observations of Gärntner (Medicinische Jahrbucher, 1884, 1) harmonize with

this. He found that radiant heat contracts the blood-vessels of the frog's mesentery.

5 The same applies to conditions which are discussed under this head in textbooks,
although they have either only a medico-legal bearing or are inconstant factors, such
as the injection of the brain in death from strangulation. I need but instance the
vascular condition of brains of criminals executed by hanging. In the case of one
where the strangulation had been slow I found an engorgement of all the vessels and
arachnoidal as well as endymal hemorrhages; in a second, where the criminal had
been carried half fainting to the drop, and death ensued quickly and without signs of
distress, the brain was decidedly anæmic.

It has been also considered best to omit treating of the collateral hyperæmia of the
brain sometimes found with erysipelas of the face and scalp. This I regard as
essentially of the same nature as the metastatic meningitis of erysipelas, if it be not in
reality a first stage of the latter.

ETIOLOGY.—An individual predisposition to cerebral congestion was

one of the unquestioned facts of the older medical writers. It
undoubtedly exists, and to-day we attribute it to inherited vascular
conditions either affecting the calibre and coats of the blood-vessels
or the vigor of the vaso-motor apparatus. I have remarked the
transmission of that weakness of the latter which underlies the
congestive phenomena of later life much more frequently in the
female than in the male sex.
It has been claimed that external refrigeration produces hyperæmia
of the brain, as of other internal organs, and that this accounts for
the greater frequency of the disorder in cold weather. Niemeyer
indeed speaks of persons who, suffering from this condition, appear
and act in such a way as to convince the laity that they are
intoxicated; and Andral, Falret, and Hammond note the occurrence
of a much larger number of cases in the winter than in the summer
months. I apprehend that the condition described by Niemeyer must
be extremely uncommon, both from individual experience and the
rarity of its mention as an independently observed fact. With regard
to the alleged greater frequency of the disorder in winter, it must be
remembered that all the three observers cited include in their
computation a number of cases in which congestion was a collateral
feature; they did not limit themselves to the disorder as spoken of
here. Certainly, the physician will see few if any persons who consult
him because of the hyperæmia-producing effects of a cold day.

The suppression of habitual discharges, of the hemorrhoidal flux,

and the cessation of menstruation are associated in many instances
with the more formidable grades of cerebral hyperæmia. Many
phenomena of so-called climacteric insanity depend on congestive
states. The sudden closure of an old ulcer or the removal of
hemorrhoids in advanced life has in some well-established instances
provoked alarming seizures not unlike those noted with paretic
dementia. The chain of proof establishing the direct influence of
physiological and pathological discharges on the vascular controlling
apparatus of the brain is most complete. Not alone cumulative
clinical observation, but the occasional happy result of therapeutical
procedure based on this supposed interdependence, support it.
Thus, the congestive cerebral state is recovered from when the
menstrual or hemorrhoidal flow is re-established, or an issue is
formed in the nape of the neck, or an old ulcer is allowed to reopen.6
6 The treatment of paretic dementia, particularly of the congestive type, is also based
on this relation. The irritating antimonial ointment and issues in the nape of the neck,
etc. have been lauded by older observers, and in two of my own cases had the best
results—in one, indeed, with established restitutio ad integrum of now nearly two
 years' duration. I am inclined to suppose that its abandonment is due to an improper
selection of cases; in the ordinary premature senility and syphilitic types such
treatment is altogether ineffective. It is applicable to but a minority of cases at best,
and to them only at an early period. It is probably to a similar form of congestion that
Bouchut refers when (“Les Nèvroses congestives de l'Encéphale,” Gazette des
Hôpitaux, 1869) he speaks of a cerebral hyperæmia developing under the mask of a
meningitis—an expression that may be allowed if understood in the same sense as
the comparison between hydrocephaloid and hydrocephalus.

The origin of most cases that are brought to the physician's attention
is more or less complicated. A business-man, lawyer, or student
suffering from worry incident to his profession, living so irregularly as
to provoke gastric disturbances, becomes afflicted with insomnia,
and in addition is also constipated. Straining at stool, he finds a dull,
heavy sensation affecting the upper part of his head; attempting to
resume his work, this is aggravated, and after a series of temporary
remissions the condition to be later described becomes continuous.
In such a case the insomnia, usually due to neural irritability, if not
aggravated by an existing dyspepsia, leads to such a one, and a
circulus vitiosus familiar to all physicians is established. Each of the
factors concerned involves strain of the cerebral vaso-motor
apparatus, but none more so than the insomnia. It is not so much the
intensity of the strain as its long duration and the exhaustion of the
centre which in sleep is supposed to be at comparative rest. This
rest is not obtained, and, in conformity to the laws of neural
exhaustion, that centre becomes morbidly irritable. Now, gastric
irritation is competent to produce a reflex influence on even the
healthy cerebral organ; to do so it must be a severe one; but with the
class of persons alluded to the slightest indiscretion in food or drink
is sufficient to set up reflex vertigo or headache. The current theory
regarding these symptoms is that they are due to stimulation of the
vaso-constrictors and ensuing cerebral anæmia; but the subjects
before us will usually be found to flush up instead of becoming pale,
as in simple vertigo a stomacho læso, or if there be initial paleness,
there is a secondary flush, as if the tired arterial muscle had become
exhausted by the effort at obeying the reflex stimulus. In addition, a
profuse perspiration sometimes breaks out on the upper part of the
body.

The influence of traumatic causes and insolation in producing a

tendency to repeated and severe cerebral congestion is recognized,
particularly among alienists. It is supposed that an abnormal
irritability of the vaso-motor apparatus is provoked by these causes.
Abundant evidences are sometimes found in the brains of such
persons of an altered state of nutrition of the brain and its
membranes, and which point in the direction of congestion.

In the conditions thus far alluded to it can be fairly assumed that the
determination of blood to the cerebral blood-vessels is more or less
active. Passive congestion due to impeded return circulation is of
secondary interest, as the primary disease, be it a pertussis or a
laryngeal, cardiac, pulmonary, or surgical condition, will constitute
the main object of recognition and management. Certain quasi-
physiological acts, as coughing, hurried breathing, holding the breath
while straining at stool, and placing the head in a dependent position
while acting in the direction of passive hyperæmia, are to be
considered in connection with the active forms of congestion which
they may momentarily aggravate.

MORBID ANATOMY.—Owing to the non-fatality of the commoner forms

of cerebral hyperæmia, no pathological observations of them are at
our disposal, nor can we assume from analogy that the appearances
would be well marked if they could be made. What little knowledge
we have is derived from a study of more serious conditions of which
cerebral hyperæmia is an initial, collateral, or episodial feature.

In pronounced cerebral hyperæmia the entire brain is, as it were,

tumefied, so that the dura appears tensely stretched over its surface
and the gyri are flattened; both the meningeal vessels proper and
those of the pia are injected. According as the hyperæmia is active
or passive the color of this injection varies, being of a brighter red in
the former, of a purple or bluish color in the latter case. The purest
instances of active cerebral hyperæmia which I have seen were
found in patients dying in the apoplectiform phases of paretic
dementia (progressive paralysis of the insane). Here the cortex on
section exhibited a beautiful rosy tint, which was distributed in darker
and lighter strata in correspondence with the distributional areas of
the short and the long cortical arteries; there were numerous puncta
vasculosa both in the cortex and in the white substance, and in some
instances the arachnoid or the ventricular fluid was tinged with blood,
albeit no vascular rupture could be discovered. The red blood-
corpuscles undoubtedly escape by diapedesis from the surface as
well as the endymal vessels; the same thing occurs in the
intracerebral blood-vessels, whose adventitial spaces are often
crowded with accumulations of red blood-discs, while groups or
single ones are found scattered in the surrounding parenchyma, and
even in the periganglionic spaces. Occasionally accumulations of
pigment found near the vascular channels remain to attest the
former existence of other hyperæmias, and indeed slight
accumulations of this kind are found in the brains of most persons
who have reached adult life. These are to be regarded as remnants
of the physiological hyperæmias to which all active individuals are
subject. It is only when the accumulations become considerable and
numerous, as in the chronic insane, or are associated with those
changes in the blood-vessels which are discussed in the articles on
thrombotic and hemorrhagic cerebral disease, that they can be
regarded as indications of a pathological condition.

Acute simple meningitis is ushered in by cerebral hyperæmia of the

active form. This is not alone demonstrated by the early symptoms of
this disease, but also by the fact, which I have observed in two
cases, that where this form of meningitis originates on one side, as
from extension of the middle-ear trouble, the opposite cerebral
hemisphere exhibited intense congestion of the ideal type.

In that serious form of mental disease known variously as grave or

acute delirium and typhomania (Luther Bell) a form of cerebral
hyperæmia is observed which in its intensity approximates
inflammatory congestion. The surface of the brain appears marbled
and mottled; blood seems to exude from the gyri after the pia is
removed; the cortical lamination is invisible, owing to the hyperæmic
discoloration of the gray substance; and the parenchymatous
elements themselves appear to be in a state of cloudy swelling. In
one case I have observed transudation of a hyaline proteinaceous
substance and an exudation of fibrin around the larger arterioles. In
some cases of typhus fever a less intense but similar congestive
hyperæmia is found. The hyperæmias of paretic dementia, of acute
delirium, and of typhus fever agree in this one feature: that all
districts of the brain, from the cortex and white substance of the
cerebral hemispheres to the medulla oblongata, are involved nearly
to the same degree. In the hyperæmia of simple meningitis of the
convexity it is chiefly confined to the pia mater and the most
superficial cortical strata.

Congestion of the brain from stagnation of the venous return

circulation should not be confounded with active hyperæmia. With
this condition, which may be due to thrombosis of the sinuses,
morbid growths near the jugular foramen or in the neck around the
internal jugular veins, or, finally, to certain cardiac and pulmonary
disorders, there is rather a lesser than a greater amount of blood
sent to the brain; and it is not infrequently found that while the
surface of the brain appears congested, owing to the prominence of
the cerebral veins, the deeper parts are quite anæmic; and if the
injection be general, it will be found that the blood, whether in
arteries or veins, has the venous character. An excellent example of
this form of congestion is afforded by persons dying in the status
epilepticus. In their brains the venous channels stand out, filled to
their extreme capacity with blood almost black in color; and in
prepared sections, particularly such as are taken from the pons and
medulla oblongata, a beautiful natural injection of the vessels is
found. But that rosy color which is so characteristic of active
hyperæmia is absent, the tissues appearing purplish, bluish, or
chocolate-colored.

SYMPTOMATOLOGY.—There are few symptoms attributable to the

nervous system which have not been enumerated among the
characteristics or the occasional manifestations of cerebral
hyperæmia. Thus, Hammond not only follows Andral in enumerating
apoplectic, convulsive, comatose, and maniacal symptoms as acute
manifestations of active cerebral congestion, but assures us that
aphasia may occur under the same circumstances. In the course of
his work on the subject, “an absolute want of power to get correct
ideas of even simple matters,” confusion of ideas, weakening of the
judgment, vacillation of purpose, diminished logical power, illusions
and hallucinations of every sense, delusions, morbid apprehension
of impending evil, imperative, suicidal, and other impulses,
suspicion, hypochondriasis, furious delirium, and the use of profane
and obscene language, are enumerated among the characteristic or
prominent symptoms of various forms and cases of cerebral
hyperæmia.7 Not one but several of the recognized forms of insanity
have yielded a fair quota of their symptoms to this long array. Among
somatic signs he in like manner names neuralgic pains, numbness,
spasms, paralysis, false impotence, hyperæmia of the tympanum,
choked disc, abolition or perversion of the sense of smell, taste, and
sight, fibrillary or fascicular twitches, various states of the urinary
excretions, diplopia, and monoplegias. It is here equally evident that
the initial symptoms of a considerable number of organic and clearly
defined affections have been included. It is on account of the
confusion engendered by this wide interpretation of the meaning of
the term congestion of the brain that I have determined to limit the
term as previously indicated, and to consider only the active form
here.
7 A Treatise on the Diseases of the Nervous System, 7th ed., pp. 1-53. The natural
inference following a perusal of this chapter, as well as the monographs to which their
author refers, is that he has gathered together all states in which cerebral hyperæmia
was an associated factor, as well as those in which he appears to assume its
existence on theoretical grounds, and designated them as cerebral congestion. In
some instances he uses the terms hypochondria and cerebral hyperæmia
interchangeably (p. 50, loc. cit.).

A feeling of head-pressure, associated with a more or less severe

dull pain, aggravated by mental exertion, by stooping down, by
straining at stool, or when out of breath, and accompanied by a
subjective sense of mental dulness, is the most constant feature of
the ordinary cases. There is usually a vertiginous sensation, and an
irritability of the eye and ear not unlike that described in the article on
Cerebral Anæmia. Sleep is at first disturbed by vivid and sometimes
frightful dreams; later, it becomes interrupted, and ultimately
complete insomnia may develop. The action of the heart is
accelerated and exaggerated in some cases; in that event increased
pulsation of the carotids, flushing of the face, injection of the
conjunctiva, and a subjective sense of heat in the head and face are
experienced. Hammond, in accord with Hasse and Krishaber,
believes that febrile symptoms may develop under these
circumstances; most authorities, however, deny this for the
uncomplicated form. I have never found an objective rise of the
general temperature.

Such a condition as that described is usually slowly produced,

several weeks, or even months, being occupied in its development.
At first the unpleasant symptoms occur only at certain hours of the
day, with temporary exacerbations and remissions. It may be
arrested with comparative ease at any time; if neglected, the mental
faculties become affected, not in the grave sense in which Hammond
and the older authors describe it, so as to carry the patient into
actual dementia or delusional insanity, but rather in the way of
diminished working-power. It is more difficult to fix attention, to
recollect words, names, and figures, or to keep up a protracted
mental effort, than in health, but the formal judgment does not suffer.
I have known patients to be in this condition for many months, and
several for more than one year, without any grave deterioration. It is
true that in the prodromal periods of some forms of insanity, such as
acute mania, there is a condition very similar to that of these
patients; and this has led to regarding mania as a possible phase of
cerebral hyperæmia. But the very fact that, typically, mania is
preceded by such a stage—which is always of brief duration—that
maniacal excitement is a constant and unavoidable consequence
upon it, while, as far as known, the condition here described may last
for years without leading to a true psychosis, should prevent one
regarding the two conditions as identical, however similar they may
be for the time being.
In sufferers from cerebral hyperæmia who pass into the chronic state
of this disorder the disturbance of sleep and of the digestive organs
becomes very prominent, and continually reinforces the acting
causes of the disorder. In a large number of cases the head-
sensations become more or less localized; that is, while the general
feeling of pressure or dull ache may continue, a special area, which
can be covered by the palm of one hand, either in the middle part or
to one side—usually the left—of that part of the vertex, is the seat of
a more severe pain, complained of as a hot pressure. The patients
frequently claim that the temperature is higher at this spot, and,
contrary to what might be anticipated on a priori grounds, the
statement will be confirmed, not alone by the coarse method of using
the hand, but by the surface thermometer. The locality where this
occasional rise of temperature and the more common sense of
pressure are experienced corresponds to that part of the longitudinal
sinus where the largest cerebral veins enter. It is a noteworthy fact
that nearly all the important admunctories of this sinus empty into it
within the short space of two inches at this point.

Not all sufferers from cerebral hyperæmia give a history of a gradual

development of their symptoms. A few date their trouble from some
single intellectual, physical, or emotional strain. In one case,
complicated by marked evidences of cerebro-spinal exhaustion, the
patient, a lady, had during an illness of her husband, being deserted
by her servants, and the water-supply having been cut off, carried all
the water required for the invalid and domestic as well as sanitary
purposes up three flights of stairs for two unusually hot days in July.
In two others, strikingly similar in many details of their cases, both
being cornet-players, both attributing their illness to an extra call
upon their instrument, it was brought on in the older patient within a
few hours after playing on a hot day at the State Camp at Peekskill,
and in the second at Narragansett Pier as he left the sultry concert-
room and became exposed to a draught. In both these cases, as in a
large number since examined, some stomach trouble could be
positively determined to have antedated these symptoms. I mention
this because it is only in such cases that I have found the nausea or
vomiting which some writers regard as an occasional occurrence of,
and due to, the lighter form of cerebral hyperæmia.

There are no ophthalmoscopic evidences of cerebral hyperæmia of

this form. I have never found the optic disc presenting variations in
tint beyond those found within normal limits, except in a case of
saturnine encephalopathy with predominant signs of cerebral
congestion. I believe that the statement of Hammond8 as to the
existence of choked disc in cerebral hyperæmia is generally
regarded as due to the interpretation of organic diseases as
congestive states. It is not confirmed by authorities.
8 Loc. cit., p. 41, lines 29-36.

I have never found the tympanic membrane hyperæmic

independently of ear disease, even when tinnitus was marked. It is
claimed to exist by Hammond, and he adduces as analogous the
observation of Roosa that quinine produces an injection around the
handle of the malleus.9
9 It certainly is not necessary to look to the injection of the tympanum as an
explanation for the tinnitus of cerebral hyperæmia, based on such an analogy. The
tinnitus of cinchonism is more central in location, being producible in persons who
have pathological or no tympanic membranes, just as the tinnitus of cerebral
hyperæmia occurs indifferently under like circumstances.

The congestive states which follow traumatism and insolation are

properly considered in connection with the traumatic neuroses and
certain forms of insanity. But there are some milder cases in which
the symptoms remain within such compass as is comprised in this
section. The patient, after a fall or a blow on the head, suffers from
insomnia, has a sensation of fulness and ache in the head,
complains of a pulsating feeling in the occipital region and an
inability to concentrate his thoughts on subjects which previously
were parts of his routine. Under appropriate treatment recovery
ensues, but there remains behind an intolerance of alcoholic
beverages, and at times the patient experiences momentary fits of
abstraction, which may be regarded as mild analogies of the more
serious episodes of the full-blown traumatic neurosis. Thus, he may
be walking along the street and suddenly lose his train of thought for
an instant, to regain it on observing that he has inadvertently made a
misstep. Or in the midst of an address a previously fluent orator in
attempting to find a certain by-law in the rules of a society is unable
to recollect which he was in search of, and is compelled to take his
seat with a rambling apology. But for the fact that similar sequelæ
are noted in cerebral hyperæmia from other causes, it would be
questionable whether it be proper to attribute them to the congestive
element engendered by the traumatic influence. They are usually
noted when the hyperæmic phenomena proper have become latent
or disappear, and, with other symptoms customarily treated of as
mere results of circulatory trouble, may be regarded as signs of
neural exhaustion or inadequacy rather than of insufficient
ensanguination.

A more serious form of cerebral hyperæmia occurs in females in

conjunction with the climacteric period, and in both sexes in
consequences of the suppression of any habitual discharge in
advanced, and exceptionally in middle and juvenile, life. The advent
of the symptoms is rapid, a few hours or days sufficing for the
development of the attack. The face is flushed, the carotids throb
violently, the general cutaneous surface is congested, and the
patient is incoherently talkative. The one side, usually the right, is
heavy and tremulous, the fingers are devoid of their usual skill, and
the speech is more or less thick. The sleep is disturbed or replaced
by a stuporous condition, whose similitude to an apoplectiform
seizure is sometimes heightened by stertorous breathing. After one
or several days the patient emerges from this condition by degrees
or suddenly with complete restitutio ad integrum. But the attack may
recur, and ultimately it is noted in the event of repeated attacks that
the return to the normal state is slower and less complete: the
disorder then undergoes a transition into the congestive type of
paretic dementia described in another portion of this volume.

DIFFERENTIAL DIAGNOSIS.—In some of its clinical aspects cerebral

hyperæmia closely resembles cerebral anæmia. This is not
surprising when we bear in mind that both constitute nutritive
disturbances of the same organ, and that, notwithstanding the
apparent difference in the surface injection of an anæmic and a
hyperæmic brain, the state of affairs in the ultimate capillary districts
may be much more alike than might be anticipated on theoretical
grounds. In congestion we have wider vessels, and perhaps, though
not necessarily, a better quality of blood; but at the same time the
intracranial pressure may be such that the venous emunctories can
labor but slowly: the result will be that although there is more blood
in the brain, the lessened rate of flow places the nerve-elements
under nearly the same nutritive disadvantage that they are placed
under with the narrower and vitiated but more rapid blood-column of
ordinary anæmia.10 It is particularly the symptoms dependent on
those nerve-centres and tracts which are, so to speak, dynamically
sensitive, which resemble each other so much that an intrinsic
difference—both being placed side by side—is not always
determinable. This is true of the aural and optic symptoms. Tinnitus,
photophobia, scotomata, and blurring or darkening of the visual field
occur in both, and in about the same varieties. In my experience the
acuteness of hearing is more apt to be interfered with by the
subjective sounds with hyperæmic than with anæmic tinnitus. The
scotomata of hyperæmia are more distinct and coarser than those of
anæmia; darkening of the visual field is more apt to occur with
sudden rising in anæmia, while in hyperæmia it is provoked by
coughing, straining at stool, or other cause operating directly or
indirectly on the return circulation. It may be stated, as a general
rule, that if any of these symptoms are aggravated on lying down or
stooping, they are due to hyperæmia; while if the same procedures
are resorted to in anæmia, amelioration ensues. But in many chronic
cases these symptoms seem to continue as indications of a
permanently altered activity of the nerve-elements themselves; that
is, as a sort of pathological habit. In that case the position test may
not be decisive. In one respect there is a decided difference between
the anæmic and hyperæmic forms; there is never amaurosis in the
latter, while it is approached, and occasionally fully developed, in the
former. Much more importance attaches to the differentiation of
tinnitus due to nutritive brain disorders and that due to aural disease.
As a rule, the tinnitus from cerebral hyperæmia is symmetrical; if
unilateral, it is of short duration. The procedure of Valsalva11
aggravates the tinnitus of hyperæmia, and relieves that which is due
to the commoner forms of ear disease; the former is aggravated and
the latter relieved by noise.
10 It is also admitted that the blood stagnating in the larger veins and accumulating in
the arteries, the limits of compressibility of the other cerebral contents being passed,
the capillaries will suffer, so that with injected and turgescent arterioles and venules
there may be capillary anæmia.

11 I would caution against Politzer's method in cases of ear disease coexisting with
cerebral congestion. In a patient now under my treatment each session at the aurist's
was followed by a distinct exacerbation of the cerebral symptoms.

In the table on p. 773 I have attempted to formulate the principal

differential relations of the protracted forms of cerebral anæmia and
hyperæmia.

There are a number of so-called functional nervous states which,

aside from the fact that they are unwarrantably confounded with
cerebral congestion, do not require mention in a differential relation.
Such are the masturbatory neurosis, certain hysterical states, and
the asthenia resulting from nervous shock and overwork. These
states have found a provisional resting-place under the
comprehensive and non-committing title of neurasthenia or nervous
exhaustion—a term which includes conditions fully recognized by
Robert Whytt and Isenflamm in the last century.

Symptomatic State. In Cerebral Anæmia. In Cerebral Hyperæmia.

Pupils. Usually dilated and mobile. Usually small or medium.
Respiration. Often interrupted by sighing or Normal.
by a deep breath, even when at
rest.
Headache. Either sharp and agonizing, and If localized, accompanied by a
then in a limited area, or a subjective and objective
general dull ache, intensified in (always?) feeling of heat; if
 the temples and over or behind general, is compared to a bursting
the eyes. or steady pressure.
Activity. There is lassitude. There is indisposition to exertion,
yet patient is restless.
Temperament. Lethargic, with exceptions. Choleric, with exceptions.
Intellect. Inability to exert. Rather confusion than inability of.
Sleep. Insomnia, interrupted by trance- Insomnia, with great restlessness,
like conditions, in which the variegated by unpleasant and
patient is comparatively confused dreams.
comfortable. Dreams often
pleasant.
Influence of upright Aggravates all the symptoms. Either without influence or
position of body. beneficial.
Influence of Amelioration. Aggravation.
recumbent position of
body and dependent
position of head.
Influence of acts If any, a sharp headache may Aggravated.
involving deep ensue, but the other symptoms
inspiration, such as are not aggravated.
blowing, straining at
stool, sneezing, etc.

TREATMENT.—Ergot of rye with its preparations may be regarded as

the cardinal drug in cerebral hyperæmia. There are few drugs in the
domain of neurological therapeutics which are so directly antithetical
to the pathological state as this one. There is scarcely a case of
cerebral hyperæmia that is brought to the physician's attention but
may be regarded as being in part due to an over-distension of the
cerebral vascular tubes. This is directly overcome by ergot, and the
quantity which such patients will sometimes bear without showing
signs of ergotism is something remarkable, in notable contrast with
the subjects of cerebral anæmia, who are usually very sensitive to it.
About three grains of Bonjean's ergotin may be regarded as a safe
trial-dose for an adult, and unless a distinct effect is produced within
two or three days this dose may be raised to six grains twice or three
times within twenty-four hours. It is not advisable to combine
strychnia with the ergotin, as is often done; the effect of that alkaloid
is to increase the psychical and sensorial irritability of the patient.
Chloral hydrate or bromide, or both in combination, is as useful an
adjuvant here as it would be hurtful in cerebral anæmia.

It is not usually necessary to employ special hypnotics in cerebral

congestion. The same drug whose beneficial effect is so potently
marked during the daytime that tinnitus, cerebral pressure, and
subjective drowsiness will disappear before it, if not as rapidly, more
enduringly, than the symptoms of cerebral anæmia disappear before
nitrate of amyl, will also overcome the insomnia in the majority of
cases. Where it fails, warm pediluvia or sitz-baths will prove more
efficient than the majority of hypnotics. Their use, at all events,
involves no hurtful effect on a—possible already—disordered
stomach, and their certainty of action is much more even. Their
temperature should be about 40-42° Centigrade, and the immersion
continue from fifteen to twenty-five minutes.12
12 A number of experiments, the most recent of which were by Musso and Bergesio
(Rivista sperimentale di Freniatria e di Medicina legale, 1885, xi. p. 124), have shown
that in such baths the cerebral pulsations become less excursive and that the volume
of the brain decreases. The same applies to general warm baths.

In those cases where the subject sensations accompanying

hyperæmia, active or passive, are intensified in the posterior
segment of the head or the nuchal region, leeches at the mastoid
process, or cupping, wet or dry according to the severity of the
symptoms, will often give immediate relief. Burning with the actual
cautery, or, what is equivalent and a much neater application, the
heated glass rod, has an equally happy effect in that class of cases
where throbbing and pain are intensified low down. It should be done
as near the spot indicated by the patient's complaints as possible.13
13 In a case of gliomatous hypertrophy of the pons oblongata transition marked by the
development of numerous tortuous and enlarged blood-vessels the episodes of the
disease were found to be of the congestive type, and yielded to no other treatment
than that with the cautery.
The diet of patients who are suffering from or subject to cerebral
hyperæmia should not be stimulating nor difficult of digestion. It is
much more important to avoid distension or overstrain of the
stomach than to reduce the nutritive value of the food in the majority
of cases, for true plethora is much less common than is supposed.
The bowels should be so regulated that the patient have at least
one, and that an easy, movement a day. The saline cathartics,
particularly the Carlsbad salt, are to be used to effect this if
necessary. The clothing around the neck should be free and not
compress the parts.

In those severe forms of cerebral congestion attending the

climacteric period, or occurring in consequence of the suppression of
discharges, and similar causes, the symptoms are often so alarming
as to render energetic measures, such as bleeding, immediately
necessary. This may be affected by applying leeches to the nose,
the temples, or by bleeding at the arm. If due to the suppression of
hemorrhoidal discharges or menstruation, the leeches should be
applied to the anus and hot sitz-baths taken. In the milder forms a pill
composed of aloes, podophyllin, and ox-gall, recommended by
Schroeder van der Kolk, will be found effective.

Cerebral Anæmia.

The oft-confirmed observation of Treviranus, that the brain is paler in

the sleeping than in the waking state, supplemented as it has been
by more elaborate observations, which show that the difference
between the intracranial blood-amounts, as estimated in these
opposite states, is equivalent to one-twenty-fourth part of the total
blood-amount of the body, has been made the basis of much
dazzling theory and premature speculation. Hyperæmia of the
central nervous apparatus or of certain of its provinces becomes
regarded as synonymous with over-activity, and anæmia, general or
provincial, as the expression of the opposite functional state.
Elaborate directions may be found, even in recent treatises on the