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 Healthy Lunch
Cookbook
Discover Healthy Lunch Recipes with an
Easy Lunch Cookbook

By
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 LEGAL NOTES
All Rights Reserved. No Part Of This Book May Be Reproduced Or
Transmitted In Any Form Or By Any Means. Photocopying, Posting Online,
And / Or Digital Copying Is Strictly Prohibited Unless Written Permission
Is Granted By The Book’s Publishing Company. Limited Use Of The Book’s
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 Table of Contents
Michelle’s Favorite Lunch 7
Sunflower Healthy Lunch 10
Coconut Cantaloupe 11
Complex Southern Fruit Salad 12
Juice Bar Fruit Salad Drink 13
Vegetarian Tofu Fruit Salad Lunch 14
Apricots and Lemon Fruit Salad with Nuts 15
Autumn Cinnamon Salad 16
Fruit Salad Sauce 17
Strawberry Sesame Salad 20
Cranberry Salad 21
Orange Romaine Salad 22
Chinese Orange Salad 23
Maggie’s Favorite Peach Yogurt Salad 24
Creamy Mushrooms with Shrimp 25
Greens, Corn, Black Beans, and Olive Brown Rice 26
Cashews, Chickpeas, and Mushroom Brown Rice 27
Buttery and Baked Brown Rice 30
Instant Lemon and Parsley Brown Rice 31
Pepper, Balsamic, Dijon, and Raisins Brown Rice 32
Peppers, Onions, and Cheddar Brown Rice 33
Easy Latin Style Rice 34
Brown Rice Risotto I 35
4
Zucchini, Chicken, Mushrooms, and Swiss Brown Rice 36
Meaty No-Meat Brown Rice Bake 37
Easy Louisiana Style Brown Rice 40
Easy Mexican Style Brown Rice 41
Black Bean and Rice Burgers 42
Chi Tan T'ang 43
Sweet and Spicy Tofu Soup 44
Easy Wonton Soup 45
Alternative Egg Drop Soup 46
Natural Ramen Noodles 47
New Classical Ramen 50
Ramen Re-Imagined 51
Super Easy Coconut Soup Thai-Style 52
Vegetable Soup In Thailand 53
A Uniquely Simple Cumber Soup with Thai Roots 54
Charong’s Favorite Thai Soup of Ginger 55
A Thai Soup of Veggies 56
Easy Coconut Soup 57
Spicy Kale and Onion Soup 60
Lemony Soy Sauce Soup 61
Japanese Mushroom Soup I 62
Japanese Mushroom Soup II 63
Kale Soup II 64
Sunbelt Quinoa Classic 65
Quinoa Festival 66
Blueberry Lunch Brunch Quinoa 67
Middle Eastern Style Quinoa 70
Cheesy Veggie Quinoa 71
Countryside Quinoa 72
Caribbean Curry Quinoa 73
Quinoa in Rome 74
Quinoa Chili 75
Mexico City Quinoa 78
Quinoa Turkey Loaf 79
Black Bean Quinoa Burgers 80
Quinoa Summer Salad 81
Quinoa in Classical Greek Style 82
Michelle’s Prep Time: 10 mins

Favorite Lunch Total Time: 35 mins

Servings per Recipe: 8

Calories 199 kcal
Fat 0.2 g
Carbohydrates < 51g
Protein 1.3 g
Cholesterol 0 mg
Sodium 130 mg

Ingredients
1 29 oz. can pear slices, drained and cut 1 20 oz. can pineapple tidbits, drained
into bite-size pieces 1 4.6 oz. package non-instant vanilla pudding
1 28 oz. can sliced peaches, drained and mix
cut into bite-size pieces with 1 C. liquid
reserved

Directions
1. Get a bowl, combine: pineapple, peaches, and pears.
2. In a pot add in the pudding mix and juice from the peaches and with a low level of heat
stir and warm the mix for 7 mins. Combine this mix with the fruits and toss everything
gently.
3. Place a covering of plastic on the bowl and put everything in the fridge for 30 mins.
4. Enjoy.

Michelle’s Favorite Lunch 7

SUNFLOWER
Healthy Lunch
Prep Time: 10 mins
Total Time: 10 mins

Servings per Recipe: 8

Calories 184 kcal
Fat 13.2 g
Carbohydrates 14.6g
Protein 4.6 g
Cholesterol 3 mg
Sodium 170 mg

Ingredients
2 C. mixed salad greens 2 tbsps flax seeds
1/4 C. ranch dressing 1/3 tsp sea salt
3/4 C. diced tomato 1/4 tsp chopped garlic
3/4 C. dried cranberries 2 tbsps grated Parmesan cheese, or to
1/2 C. sunflower seeds taste
1/3 C. almonds

Directions
1. Get a salad bowl, combine: dressing and greens. Toss the greens to get them mixed well.
Combine in the garlic, tomato, sea salt, cranberries, flax seeds, almonds, and sunflower
seeds. Toss the salad gently then garnish everything with the parmesan and stir.
2. Enjoy.

10 Sunflower Healthy Lunch

Coconut Prep Time: 15 mins

Cantaloupe Total Time: 15 mins

Servings per Recipe: 8

Calories 82 kcal
Fat 1g
Carbohydrates 19.2g
Protein 1.1 g
Cholesterol 0 mg
Sodium 21 mg

Ingredients
1 cantaloupe - peeled, seeded, and cubed 1/4 C. sweetened flaked coconut optional
2 red apples, thinly sliced
1 C. red grapes
1 12 oz. can mandarin oranges in juice

Directions
1. Get a salad bowl and layer in it half of the following: cantaloupe, mandarins, apple, and
grapes. Continue add the rest of ingredients in the same manner.
2. Add your coconut over everything as a topping.

Coconut Cantaloupe 11
COMPLEX
Southern Fruit
Prep Time: 25 mins
Total Time: 55 mins

Salad Servings per Recipe: 10

Calories 398 kcal
Fat 27.1 g
Carbohydrates 40.6g
Protein 3.7 g
Cholesterol 8 mg
Sodium 151 mg

Ingredients
3 bananas, peeled and cut into chunks
1 13.25 oz. can pineapple chunks,
drained
2 red apples, cored and cut into bite-
sized pieces
2 Granny Smith apples, cored and cut
into bite-sized pieces
2 kiwi fruit, peeled and cut into chunks
3 oranges - peeled, segmented, and cut
into bite-sized pieces
2 tangerines, peeled and segmented
1 C. mayonnaise
1 4 oz. jar maraschino cherries, drained
and juice reserved
1/2 8 oz. package chopped walnuts, or to
taste
1/2 C. chopped celery, or more to taste
1/2 3.5 oz. package sweetened flaked
coconut, or more to taste

Directions
1. Get a bowl, combine: coconut, bananas, celery, pineapple, walnuts, red apples, cherries,
granny smith, mayo, kiwi, tangerines, and oranges.
2. Toss the salad gently then add in the cherry juice that was reserved and toss everything
again. Place a covering on the bowl and put everything in the fridge for 1 hr.
3. Enjoy.

12 Complex Southern Fruit Salad

Juice Prep Time: 10 mins

Bar Fruit Salad Drink Total Time: 10 mins

Servings per Recipe: 6

Calories 104 kcal
Fat 1.9 g
Carbohydrates 19.7g
Protein 3.4 g
Cholesterol 7 mg
Sodium 38 mg

Ingredients
2 C. milk 4 strawberries, chopped
1 8 oz. can pineapple tidbits 1/4 C. cherries, pitted and chopped, or to taste
1 apple, chopped 2 tbsps vanilla yogurt, or more to taste
1 pear, chopped

Directions
1. Add the following to your food processor and puree it: yogurt, milk, cherries, pineapple,
strawberries, pear and apple.
2. Once the mix is smoothie like, should be 6 mins of processing, pour the smoothies into
serving glasses, recipes makes about 6 servings.
3. Enjoy.

Juice Bar Fruit Salad Drink 13

VEGETARIAN
Tofu Fruit Salad
Prep Time: 30 mins
Total Time: 55 mins

Lunch Servings per Recipe: 8

Calories 168 kcal
Fat 6.9 g
Carbohydrates 19.2g
Protein 9.6 g
Cholesterol 2 mg
Sodium < 325 mg

Ingredients
1/2 C. white rice 1/2 C. diced celery
2 C. extra-firm tofu, drained and cubed 3 tbsps diced green onions
1 C. yogurt 1/4 C. walnuts
2 tbsps lime juice salt and pepper to taste
1 tbsp curry powder
1 C. halved grapes
1 tbsp dried cranberries

Directions
1. Get your water boiling in a larger pot then once it is add in the rice. Place a lid on the pot,
set the heat to low, and let everything cook for 22 mins, then shut the heat.
2. Begin to get another pan of water boiling then place your tofu in it to cook for 4 mins.
Remove all the liquid and let the tofu lose its heat.
3. Get a bowl, combine: curry powder, lime juice, and yogurt. Work the mix until it is
completely combined.
4. Now get a 2nd bigger bowl, combine: tofu, grapes, rice, cranberries, walnuts, green onions,
and celery.
5. Toss the rice fruit salad with your lime dressing then add some pepper and salt.
6. Enjoy.

14 Vegetarian Tofu Fruit Salad Lunch

Apricots Prep Time: 20 mins

and Lemon Fruit Total Time: 50 mins

Salad with Nuts Servings per Recipe: 8

Calories 232 kcal
Fat 5.3 g
Carbohydrates 46.2g
Protein 1.7 g
Cholesterol 0 mg
Sodium 190 mg

Ingredients
1 3 oz. package lemon pudding mix 1 C. sliced apricots
1 15.5 oz. can mandarin oranges, drained 1 kiwis, peeled and sliced optional
with liquid reserved 1/2 C. chopped cashews optional
3 bananas, sliced

Directions
1. Get a bowl and mix the juice from the oranges with the pudding mix. Work the mix until
it smooth then combine in the cashews, bananas, kiwi, and apricots. Place a covering of
plastic on the bowl and put everything in the fridge until it is cold.
2. Enjoy.

Apricots and Lemon Fruit Salad with Nuts 15

AUTUMN
Cinnamon Salad
Prep Time: 15 mins
Total Time: 13 hrs 45 mins

Servings per Recipe: 4

Calories 263 kcal
Fat 5.4 g
Carbohydrates 55.9g
Protein 2.6 g
Cholesterol 0 mg
Sodium 13 mg

Ingredients
8 prunes pitted prunes 1 apple, cored and chopped
1/4 C. dried apricots 1/2 C. orange juice
1 C. apple juice 3 tbsps orange marmalade
1 cinnamon stick 1/4 C. chopped pecans
1/2 tsp whole cloves
1 banana, peeled and sliced
1 large orange, peeled, sectioned, and
cut into bite-size

Directions
1. Get the following boiling in pot: cloves, prunes, cinnamon, apple juice, and apricots. Once
the mix is boiling shut the heat and let the mix stand for about 7 hours.
2. Take out the dried fruit from the mix then separate the orange, prunes, banana, and
apricots between 4 serving platters.
3. Run the orange marmalade, orange juice, and apple juice from a strainer then garnish the
servings with the resulting liquid.
4. Garnish each serving finally with the nuts.
5. Enjoy.

16 Autumn Cinnamon Salad

Fruit Salad Prep Time: 5 mins

Sauce Total Time: 5 mins

Servings per Recipe: 16

Calories 110 kcal
Fat 5.1 g
Carbohydrates 14g
Protein 2.4 g
Cholesterol 15 mg
Sodium 39 mg

Ingredients
8 oz. sour cream 1/4 tsp ground cinnamon, or to taste
1 14 oz. can sweetened condensed milk 1/4 tsp ground cardamom, or to taste
1 tsp vanilla extract
1/2 tsp almond extract

Directions
1. Get a bowl, combine: cardamom, sour cream, cinnamon, condensed milk, almond extract,
and vanilla. Whisk the mix completely then place a covering of plastic on the bowl and
put everything in the fridge as a dressing for any salad of fruit.
2. Enjoy.

Fruit Salad Sauce 17

STRAWBERRY
Sesame Salad
Prep Time: 10 mins
Total Time: 1 hr 10 mins

Servings per Recipe: 4

Calories 491 kcal
Fat 35.2 g
Carbohydrates 42.9g
Protein 6g
Cholesterol 0 mg
Sodium 63 mg

Ingredients
2 tbsps sesame seeds 10 oz. fresh spinach - rinsed, dried and
1 tbsp poppy seeds torn into bite-size pieces
1/2 C. white sugar 1 quart strawberries - cleaned, hulled
1/2 C. olive oil and sliced
1/4 C. distilled white vinegar 1/4 C. almonds, blanched and slivered
1/4 tsp paprika
1/4 tsp Worcestershire sauce
1 tbsp minced onion

Directions
1. Get a bowl, combine: onion, sesame seeds, Worcestershire, poppy seeds, paprika, sugar,
vinegar, and olive oil.
2. Place a covering of plastic around the bowl, and put everything in the fridge for 65 mins.
3. Get a 2nd bowl, combine: almonds, spinach, and strawberries.
4. Combine both bowls and place the combined mix in the fridge for 20 mins.
5. Enjoy.

20 Strawberry Sesame Salad

Cranberry Prep Time: 10 mins

Salad Total Time: 20 mins

Servings per Recipe: 8

Calories 338 kcal
Fat 23.5 g
Carbohydrates 30.4g
Protein 4.9 g
Cholesterol 4 mg
Sodium 58 mg

Ingredients
1 tbsp butter 2 tsps minced onion
3/4 C. almonds, blanched and slivered 1/4 tsp paprika
1 lb spinach, rinsed and torn into bite-size 1/4 C. white wine vinegar
pieces 1/4 C. cider vinegar
1 C. dried cranberries 1/2 C. vegetable oil
2 tbsps toasted sesame seeds
1 tbsp poppy seeds
1/2 C. white sugar

Directions
1. Toast your almonds in butter for 7 mins then place them to the side.
2. Get a bowl, combine: veggie oil, sesame seeds, cider vinegar, poppy seeds, wine vinegar,
sugar, paprika, and onions.
3. Combine in the cranberries, almonds, and spinach and toss the contents.
4. Enjoy.

Cranberry Salad 21
ORANGE
Romaine Salad
Prep Time: 15 mins
Total Time: 15 mins

Servings per Recipe: 4

Calories 332 kcal
Fat 16.7 g
Carbohydrates 47g
Protein 4.9 g
Cholesterol 0 mg
Sodium 168 mg

Ingredients
1/2 C. orange juice 1 large head romaine lettuce - torn,
3 tbsps olive oil washed and dried
2 tbsps red wine vinegar 3 (11 oz.) cans mandarin oranges
1/2 tsp ground black pepper 1/2 C. slivered almonds
1/4 tsp salt

Directions
1. Get a bowl, combine: salt, orange juice, pepper, olive oil, and vinegar.
2. Get a 2nd bigger bowl, combine: orange and romaine.
3. Combine both bowls and add the almonds.
4. Enjoy.

22 Orange Romaine Salad

Chinese Prep Time: 25 mins

Orange Salad Total Time: 25 mins

Servings per Recipe: 5

Calories 397 kcal
Fat 26.8 g
Carbohydrates 38.2g
Protein 4g
Cholesterol 0 mg
Sodium 509 mg

Ingredients
1/2 C. vegetable oil 1 head red leaf lettuce - rinsed, dried and torn
1/4 C. cider vinegar 1 red onion, diced
1/4 C. white sugar 1 C. diced celery
2 tsps dried parsley 2 (11 oz.) cans mandarin orange segments,
1 tsp salt drained
1 pinch ground black pepper
1/2 C. sliced almonds
1/4 C. white sugar

Directions
1. Get a Mason jar, combine: pepper, oil, salt, vinegar, parsley, and sugar.
2. Place a lid on the jar and shake the contents. Then put everything in the fridge.
3. Toast your almonds with the sugar until the sugar melts and coats the nuts.
4. Let the almonds cool then break them into pieces.
5. Get a bowl, combine: almonds, lettuce, orange, and celery. Add in the dressing and stir the
mix to evenly distribute the dressing.
6. Enjoy.

Chinese Orange Salad 23

MAGGIE’S
Favorite Peach
Prep Time: 10 mins
Total Time: 10 mins

Yogurt Salad Servings per Recipe: 6

Calories 141 kcal
Fat 0.5 g
Carbohydrates 33.2g
Protein 3.3 g
Cholesterol < 1 mg
Sodium < 32 mg

Ingredients
3 large peaches, peeled and cut into 3 tsps lemon juice
chunks
1 1/2 C. blueberries
1 1/2 C. sliced strawberries
2 bananas, sliced

Directions
1. Get a bowl, combine: lemon juice and fruit.
2. Get a 2nd bowl, combine: concentrate and yogurt.
3. Combine both bowls and add a garnishing of mint.
4. Enjoy.

24 Maggie’s Favorite Peach Yogurt Salad

Creamy Prep Time: 20 mins

Mushrooms with Total Time: 35 mins

Shrimp Servings per Recipe: 6

Calories 317 kcal
Fat 6.3 g
Carbohydrates 43g
Protein 23.8 g
Cholesterol 173 mg
Sodium 1136 mg

Ingredients
2 C. instant brown rice 2 C. broccoli florets
1 3/4 C. water 1 C. baby carrots
6 tbsps soy sauce 1 small white onion, chopped
6 tbsps water 1/2 tsp black pepper
1/4 C. honey 1 C. sliced fresh mushrooms
2 tbsps cider vinegar 1 1/2 lbs uncooked medium shrimp, peeled
2 tbsps cornstarch and deveined
2 tbsps olive oil
2 cloves garlic, chopped

Directions
1. Get a bowl, mix: cornstarch, soy sauce, vinegar, honey, and water.
2. For 8 mins, in the microwave, cook your rice in 1 3/4 C. of water. Then stir it.
3. Stir fry your garlic in olive for 1 min then add in: black pepper, broccoli, onions, and
carrots.
4. Continue frying for 7 more mins.
5. Then add the mushrooms and cook for 4 more mins.
6. Empty the pan.
7. Add in your cornstarch mix to the pan and cook it for 1.5 mins then add in your shrimp.
Cook the shrimp for 4 mins before pouring in the veggies with the shrimp and reheating
everything.
8. Serve the rice with the veggies and shrimp.
9. Enjoy.

Creamy Mushrooms with Shrimp 25

GREENS, CORN,
Black Beans, and
Prep Time: 10 mins
Total Time: 2 hrs

Olive Brown Rice Servings per Recipe: 24

Calories 87 kcal
Fat 1.7 g
Carbohydrates 16g
Protein 2.6 g
Cholesterol 0 mg
Sodium 340 mg

Ingredients
1 1/2 C. uncooked brown rice 1 (4 oz.) can chopped green chilies
3 C. water 1 (4 oz.) can sliced black olives
1 tbsp extra virgin olive oil 1 (14.5 oz.) can Italian-style tomatoes,
1/2 tsp salt undrained and chopped
1 (14.5 oz.) can collard greens, drained salt and freshly ground black pepper to
1 (15 oz.) can black beans, rinsed and taste
drained
1 (15 oz.) can green peas, rinsed and
drained
1 (15.25 oz.) can corn kernels, drained

Directions
1. Boil: .5 tsp of salt, rice, olive oil, and water.
2. Once everything is boiling place a lid on the pan, set the heat to low, and let the contents
cook for 17 mins.
3. Then pour everything into a bowl and stir.
4. Place the bowl in the fridge until room temp.
5. Once the rice is room temp add the following to it, then toss: pepper, collard greens, salt,
beans, tomatoes, peas, olives, corn, and chilies.
6. Enjoy at room temp or slightly warm.

26 Greens, Corn, Black Beans, and Olive Brown Rice

Cashews, Prep Time: 10 mins

Chickpeas, and Total Time: 1 hr 20 mins

Mushroom Brown Servings per Recipe: 4

Rice (Pilaf I)
Calories 409 kcal
Fat 17.1 g
Carbohydrates 54g
Protein 12.5 g
Cholesterol 116 mg
Sodium 653 mg

Ingredients
1 1/2 C. water 2 eggs, beaten
1/2 tsp salt freshly ground black pepper
3/4 C. uncooked brown rice 1/4 C. chopped fresh parsley
3 tbsps butter 1/4 C. chopped cashews
1 1/2 C. chopped onion
1 clove garlic, minced
2 carrots, sliced
2 C. fresh sliced mushrooms
1 C. chickpeas

Directions
1. Boil your rice in 1.5 C. of water for 47 mins, in a covered pot over low heat.
2. Halfway through the rice’s cooking time, begin to stir fry your onions in butter until
tender then combine in: carrots and garlic and fry for 6 more mins.
3. Add the mushrooms and cook for 11 mins before adding the chickpeas and frying for 2
more mins.
4. Cook your eggs in a pan after the rice is done and then add to them: nuts, parsley, and
pepper.
5. Combine the rice with the eggs and also the veggies.
6. Serve everything topped with some soy sauce.
7. Enjoy.

Cashews, Chickpeas, and Mushroom Brown Rice 27

Another random document with
no related content on Scribd:
current, and it should be used in the way that will produce the
greatest amount of excitation in the cutaneous end-organs. This is
best done by applying the faradic current to the dry skin with the
metallic brush, or by allowing the cathode of the galvanic current to
rest upon it for some time.

The PROGNOSIS in peripheral anæsthesia is in the main favorable, but

it must, of course, depend much on the gravity of the lesion causing
it, as mechanical injury, pressure, neuritis, cold, etc. Rheumatic
anæsthesia, the result of exposure to cold, is in general readily
recovered from. Vaso-motor anæsthesia yields in most cases without
difficulty to treatment. Washerwoman's anæsthesia and allied cases
are intractable, and often resist the patient and well-conducted
application of remedies.

As a concrete picture of peripheral anæsthesia we will give a

description of anæsthesia of the fifth nerve—the rather that in its
consideration we meet with some of the most interesting and
important complications occurring in connection with paralysis of
sensitive nerves. The fifth nerve may have either of its three
branches separately affected, giving rise to anæsthesia limited to the
distribution of that branch, or all of its fibres may be simultaneously
involved, giving rise to complete anæsthesia of the nerve. In the
latter case the lesion of the nerve in all likelihood exists at some
point of its course between the apparent origin from the pons and the
ganglion of Gasser, which rests upon the apex of the petrous portion
of the temporal bone. Beyond this point the nerve divides into its
three branches. Amongst the causes of trigeminal anæsthesia are
injuries, tumors, syphilitic thickening of the dura mater, neuritis, etc.,
affecting the nerve within the cranial cavity. In complete anæsthesia
of the fifth nerve the parts implicated are the skin of the forehead to
the vertex, the nose, the lips, and chin up to the median line, the
cheek and temporal region, including the anterior portion of the ear,
the conjunctiva, the mucous membrane of the nose, the mucous
membrane of the mouth, and partly of the fauces of the same side.
The tongue is deprived not only of common sensation on the
affected side in its anterior two-thirds, but the sense of taste is also
lost over the same region, by reason that the fibres of the chorda
tympani, the nerve of taste for this region of the tongue, are derived
from the fifth nerve. If the whole thickness of the nerve-trunk is
involved, including the small motor root, there is, in connection with
the anæsthesia, paralysis of the muscles of mastication on the side
affected, which may be distinguished by the want of hardening of the
masseter when the jaws are forcibly brought together, and by the
thrusting of the chin over to the paralyzed side when the mouth is
widely opened, caused by the want of action of the external
pterygoid muscle, which allows the condyle on the paralyzed side to
remain in the glenoid fossa, while the condyle of the opposite side is
pulled forward upon the articular eminence by the sound pterygoid.
The face is of a dusky or livid color, and cooler than natural. Ulcers
of a stubborn character in the mucous membrane of the cheek may
be caused by the patient unconsciously biting the insensitive parts.
An inflammation of the conjunctiva is frequently set up, which may
extend to the cornea, causing ulceration, perforation,
panophthalmitis, and destruction of the eye (ophthalmia neuro-
paralytica). This has been regarded by some as caused by trophic
changes in the tissues, the direct result of irritation or destruction of
trophic fibres connected with the ganglion of Gasser. Experiments
made upon animals, however, seem to show that the inflammation of
the eye depends upon the irritation caused by the intrusion of foreign
bodies, which, owing to the loss of sensation, are not appreciated,
and which from loss of reflex action are not removed by winking nor
washed away by an increased lachrymal secretion, as in the healthy
eye. It may be that although the latter is the true explanation of the
origin of the inflammation, nevertheless the tissues may have lost
their normal power of resistance to its invasion by reason of nutritive
changes consequent upon the lesion of trophic fibres running in the
trunk of the nerve. The reflexes ordinarily induced by irritation of the
parts in their normal state are lost. Irritation of the conjunctiva causes
no winking of the lids nor secretion of tears, and titillation of the
nostrils no movements of the muscles of the face nor mucous or
lachrymal secretion. The movements of the face are less lively on
the affected side, not on account of paralysis of the muscles, but
from the loss of that constant play of reflex activity in them which
takes place in the normal condition. The loss of the reflexes
distinguishes peripheral trigeminal anæsthesia from that of cerebral
origin, in which they may still be excited by irritating the anæsthesic
surfaces. In trigeminal anæsthesia, which sometimes occurs from
the effect of cold upon the surface of the face, the mucous surfaces
are not affected.

The SYMPTOMS and DIAGNOSIS of peripheral paralysis having been

already given under the heads of Injuries of Nerves and Neuritis, a
consideration of the distribution of any motor nerve will enable us to
anticipate the distinguishing features of the paralysis dependent
upon it. With each the picture will be modified according to the
position of the muscles paralyzed and the motor functions destroyed.
It now remains to give the symptoms, diagnosis, and treatment of the
paralysis of an individual motor nerve, which may serve as an
example and paradigm, in the consideration of which points of
interest and instruction may be touched upon applicable to all other
cases.

Peripheral Paralysis of the Facial Nerve (Bell's Paralysis).

Of all the peripheral paralyses, probably that of the seventh is the

one we are most frequently called upon to treat and the symptoms of
which are the most complex and interesting. The frequency of its
paralysis is due to the length and peculiarity of its course, enclosed
as it is in a bony canal which permits no increase of its volume
without compression, the run of its terminal branches through parts
liable to inflammation and disease (parotid gland), and their final
distribution to parts exposed to all vicissitudes of heat and cold and
in constant danger of mechanical injury. The complexity and interest
of the symptoms of its paralysis depend in a great measure upon the
intimate connections it forms at different points of its course with the
fibres of other nerves of entirely different functions (acoustic and
fifth).
The seventh nerve is liable not only to intercranial compression from
tumors, inflammation of the meninges, syphilitic processes, etc., but
its long course through the petrous portion of the temporal bone
renders it liable to injury from fracture or caries, and its close
proximity to the middle ear causes it often to suffer from the
diseased conditions of the bony walls or mucous lining membrane of
that chamber, its paralysis being not infrequently the result of simple
aural catarrh. After the exit of the nerve from the stylo-mastoid
foramen it is imbedded in the parotid gland, and sometimes suffers
from compression produced by an inflammation or abscess in that
organ or by enlarged lymphatic glands in the neighborhood. Surgical
operations, so often demanded for disease of the bones or soft parts
of the face, may necessitate the lesion of its trunk or branches. The
exposed position of this nerve is sometimes the occasion of its injury
at the very outset of the life of the individual, when the application of
the forceps to the head has been resorted to in delivery. But the
most frequent cause of facial paralysis appears to be the exposure
of one side of the face directly to cold—as sleeping in a draught of
air, sitting at the open window of a railroad coach, etc. Here the
causal connection appears evident from the rapidity with which the
paralysis usually follows, although cases occur in which an interval
of hours or days elapses after the exposure before the paralysis
declares itself. Although this is usually designated rheumatic
paralysis, there is nothing to connect it with that disease, nor are
rheumatics more liable to it than others. Under such circumstances
the paralysis is probably brought about by the occurrence of a
neuritis of the nerve-trunk, which is compressed by the hyperæmia,
and it may be by an inflammatory exudation against the bony walls
surrounding it, until not only does it lose the power of conduction, but
its fibres undergo the degenerative process. In some cases the
neuritis thus excited by exposure to cold attacks the nerve after it
has issued from the bony canal, and then the resulting injury to the
fibres is much less grave. Although in some cases there are
prodromal symptoms, as stiffness or pain in the face, generally the
paralysis occurs suddenly, very often being first observed upon
awaking. The patient may be first made aware of the paralysis by an
inability to drink without the fluid dribbling from the affected side of
the mouth or by the overflow of tears from the eye of the same side.
When the paralysis is recent and the face in complete repose, there
may be little or no deformity to mark the condition of the muscles.
When, however, the patient speaks or the slightest emotional or
reflex movements of the face are excited, as laughing, frowning, etc.,
it becomes obvious from the bizarre grimace caused by a one-sided
contraction. After the paralysis has existed for some time the
contrast of the two sides of the face is marked. The paralyzed side is
characterized by a vacancy of expression to which the staring,
unwinking eye contributes. From loss of the tonicity of the muscles
the angle of the mouth droops, and the expressive furrows and lines
about the brow, below the eye, and beside the nose are smoothed
out and obliterated. Speech is affected, inasmuch as the paralysis of
the lip interferes with the pronunciation of the labials, and all
attempts to purse up the mouth, as in whistling, is abortive. The eye
not only remains open, the lids motionless, but there is partial
eversion of the lower lid (lagophthalmos), and the tears, no longer
directed to the punctum (paralysis of Horner's muscle), flow over the
cheek. The natural impulse to reflex winking caused by evaporation
from the conjunctiva or by the contact of particles of dust is
answered by a rolling of the eyeball upward to wipe the cornea
beneath the momentarily relaxed and drooping upper lid. Excited
respiration causes no movement of the ala of the nose on the
affected side, but in deep inspiration, in contrast to the normal
elevation of the ala, it is flattened down by the suction of the
inrushing current of air. In masticating, the cheek bulges out from
want of power in the paralyzed buccinator to press the food inward
against the opposing movements of the tongue. In persons who
have the rather unusual power of voluntarily moving the ear we may
detect the paralysis of the muscles concerned in those movements—
a useful point in diagnosis. Moreover, on the sound side of the face
the features have not entirely the natural appearance. The angle of
the mouth is drawn upward and the naso-labial line more deeply
impressed than natural. This results not from excessive contraction,
but from the muscles remaining in the position they have taken
during contraction, the antagonistic tonic traction from the opposite
side, which would have restored them to their normal position, being
wanting. This may be in a measure remedied by mechanical
appliances which will keep up an elastic pull from the paralyzed side,
or by restoring the muscles after contraction to position with the
hand. The tongue rests symmetrically in the floor of the mouth, and
is thrust out straight, although in appearance it is pushed toward the
side paralyzed—a deceptive appearance produced by the
asymmetrical position of the mouth. In some cases there is partial
paralysis of the velum palati, the half arch on the affected side
hanging lowest, and if we cause the patient to make the sound of ah
the opposite side of the palate is alone drawn upward. The uvula
may also participate in the paralysis, but the explanation of its
position, sometimes directed away from, sometimes toward, the side
of the paralysis, cannot be given. In proportion to the amount of the
paralysis of the soft palate will be the prominence of the symptoms
caused by it, such as difficulty in deglutition, a nasal tone in
speaking, and the escape of fluids through the nostril in swallowing.
The sense of hearing is often affected coincidently with facial
paralysis. Thus by reason of their close juxtaposition the same cause
may in common affect the acoustic and the facial, causing imperfect
hearing, subjective noises, etc. The hearing is frequently affected by
diseased conditions of the middle ear, which also cause a facial
paralysis. Still another defect of hearing, however, is caused by the
paralysis of the facial nerve itself. The stapedius muscle, supplied by
a branch of the facial, is the antagonist of the tensor tympani, and
when it is paralyzed the over-tense tympanic membrane vibrates
more readily to sound-waves, and a condition of uncomfortably
exaggerated sensitiveness to sounds is the result (hyperacuisis).
The rarely-occurring symptom of dryness of the mouth on the side of
the paralysis receives its explanation in the well-known fact of the
presence of secretory fibres for the salivary gland in the chorda
tympani, which are derived from the facial. We observe sometimes,
in connection with facial paralysis, that the patient complains of
certain subjective sensations of taste, as sour or metallic, and an
examination will in some cases reveal that the sense of taste is lost
on the anterior two-thirds of the tongue on the side of the paralysis.
The fibres which convey the sense of taste pass centripetally from
the tongue in the chorda tympani nerve, join the facial just within the
stylo-mastoid foramen, and continue united with it to the geniculate
ganglion of the facial, at which point they leave it to pass in the great
superficial petrosal to the spheno-palatine ganglion, and thence to
the trunk of the fifth nerve. Loss of sensation over the face only
occurs in cases where the fifth nerve has been simultaneously
affected with the facial, which may occur from exposure to cold.

It is obviously of importance in cases of facial paralysis to determine

if they are of central or peripheral origin. The most prominent
symptoms which mark a peripheral paralysis are the implication of all
the branches of the nerve, the loss of the reflexes, the development
of the degenerative reaction, and atrophy of the muscles. In facial
paralysis of cerebral origin the frontal and orbital branches are not at
all or but slightly affected, leaving the eye with its natural
appearance, in contrast to the lagophthalmos, and the open eye
which does not close even in sleep. In cerebral paralysis the reflexes
are normal and the muscles retain their natural electric reaction.
Accompanying brain symptoms assure the diagnosis. In facial
paralysis of bulbar origin the electric reactions are diminished, and
we have a complex of symptoms made up in a great measure by the
implication of neighboring nerves. After the diagnosis of a peripheral
facial paralysis has been made, by a careful consideration of the
symptoms we may with more or less accuracy determine at which
point of the nerve the lesion is situated. If there is paralysis of all the
muscles of the face, without alteration of taste or hearing, the electric
reaction of nerve and muscles normal, the nerve is affected outside
of the stylo-mastoid foramen. This is usually the form of slight
rheumatic paralysis. If we discover that the muscles of the external
ear are paralyzed, it shows that the point of lesion is just within the
stylo-mastoid foramen, where the posterior auricular branch is given
off from the facial. If with paralysis of the face there is alteration of
the sense of taste, with dryness of the mouth, without interference
with hearing, the trunk of the nerve is affected within the Fallopian
canal, involving the chorda tympani fibres below the point where the
stapedius nerve is given off. If to the above symptoms there is added
over-sensitiveness to sounds, hyperacuisis, and there is no paralysis
of the palate, we have the nerve affected still higher up, but below
the geniculate ganglion. If the geniculate ganglion is involved, there
is, in addition to the foregoing, symptoms of paralysis of the palate.
If, now, the lesion is above the geniculate ganglion, we will have
eliminated the symptom due to implication of the chorda tympani,
which leaves the trunk of the facial at the geniculate ganglion, and
the sense of taste is unaffected, while there remains paralysis of the
face, dryness of the mouth (the secretory fibres run in the trunk of
the seventh), hyperacuisis, and paralysis of the palate.

It was in facial paralysis that the first observations upon the

degenerative reaction in muscles were made, and it is in that
affection that these electric phenomena have been best studied, and
give us the clearest indications for prognosis and treatment in
peripheral paralysis generally. In rheumatic facial paralysis, the most
common form of peripheral facial paralysis, the electric reactions of
the paralyzed muscles enable us to classify the cases into three
groups, the prognosis and duration of which vary very much. In the
first group are the slight forms of facial paralysis. Here the faradic or
galvanic current, applied to nerve or muscles, causes an ordinary
contraction; the electric reactions are normal. These cases scarcely
require treatment, and recover in two or three weeks. In a second
group are those cases in which within a short time after the invasion
of the paralysis (two weeks) complete degenerative reaction is
observed. This degenerative reaction, with the accompanying
anatomical changes in nerve and muscle, has already been treated
of in this article, and it is sufficient here to say that it is marked by
total loss of electric excitability, both faradic and galvanic, in the
nerve, loss of faradic and increased galvanic excitability in the
paralyzed muscles, with a reversal of the normal reply of the
muscles to the different poles of the galvanic battery. These cases
constitute the severe form of rheumatic facial paralysis, and the
prognosis is grave, recovery takes place only after months, and even
after the lapse of years traces of the disease remain in the imperfect
action of the muscles. A third group of cases are of a gravity
intermediate between these two. In them is present the milder form
of degenerative reaction; that is, there is a diminution, but not a total
loss, of electric excitability in the nerve for both the galvanic and
faradic currents; but in the muscles there is a marked increase of
galvanic excitability, with qualitative change—i.e. greater contraction
upon application to them of the positive than of the negative pole.
These cases may be expected to recover in from four to eight
weeks, the muscles still exhibiting the degenerative reaction after
voluntary motion has returned. Among the symptoms to be
particularly noticed in the progress of the severe forms of facial
paralysis are spasmodic twitchings or spasms of the muscles on the
affected side of the face, about the angle of the mouth, and around
the eye, occurring spontaneously or when voluntary movements are
made. Also a state of tonic contraction and rigidity may develop in
some of the muscles, causing a permanent elevation of the angle of
the mouth, a narrowing of the opening of the eye, or a rigidity of the
cheek. These symptoms have been erroneously attributed to the use
of electricity in the treatment, but they occur as frequently in cases in
which it has not been employed. Traumatic facial paralysis, as from
wounds, surgical operations, use of the forceps in delivery, or
paralysis from compression of the nerve, as from tumors, syphilitic
thickening of the dura mater, etc., do not require a detailed mention
here, as such cases come under the head of nerve-injuries, already
discussed. Paralysis of both facials (diplegia facialis), in so far as it is
caused by peripheral nerve lesion, is an accidental occurrence, and
need not be considered as a separate form of facial paralysis. It is
often the result of central disease.

The TREATMENT of peripheral facial paralysis must begin with the

effort to remove its cause. If syphilis is suspected, mercury and
iodide of potassium must be freely used. If the cause is an affection
of the middle ear, this must be treated. Wounds or traumatic injuries
must receive the necessary surgical attention. In addition, in such
cases electricity must be employed in the manner presently to be
described. In cases of rheumatic facial paralysis the treatment will
vary with their gravity. In the lighter form in which the nerve is
affected outside of the Fallopian canal, recovery takes place in a
comparatively short time, even without treatment, but is hastened by
the use of the faradic or galvanic current daily along the branches of
the nerve. In the severe form we must open the treatment by an
attempt to combat the condition of inflammation—of inflammatory
exudation—which we suppose exists within the Fallopian canal.
Local blood-letting by leeching upon the mastoid process may be
appropriately used in the very first outset of the paralysis. Iodide of
potassium, given persistently in large doses during the earlier period
of the disease, appears to act beneficially independently of any
syphilitic taint. Electricity is the remedy, however, on which most
reliance is to be placed in the treatment of rheumatic facial paralysis,
and the manner of its application may be taken as a model of how it
should be employed in all cases of peripheral paralysis. The galvanic
current, on account of its power of penetrating to the deeper parts
and its catalytic action, is to be preferred for the direct electrical
treatment of the nerve which should be instituted in recent cases. Its
action is best obtained by placing the positive pole behind the ear on
the affected side, the cathode behind the opposite ear, and passing
a moderate current across the base of the skull (the affected nerve
being thus in the course of the current) for one or two minutes.
Occasionally the position of the poles may be reversed. Besides this
direct application of galvanism to the point of lesion, it is necessary
to make a peripheral application of electricity to the branches of the
nerve and to the paralyzed muscles. For this we use both the faradic
and galvanic currents. The galvanic current is used by applying the
positive pole stationary behind the ear, while the negative pole, with
an electrode of suitable size, is stroked over each branch of the
nerve and applied to each muscle, a current being used sufficiently
strong to produce decided contractions. This peripheral application
should be made once daily, the time of application being from two to
five minutes. The application of the faradic current is made by simply
placing one electrode upon an indifferent spot, and moving the other
over the face, with a current strong enough to cause contractions if
the muscles still respond to it, or if they do not of such strength as
the patient can bear without discomfort. Without doubt, one of the
beneficial effects of peripheral electrization is the reflex excitement of
the facial above the point of lesion through the irritation of the
terminations of the fifth nerve in the skin. A certain advantage
derived from it is that it maintains the tone of the paralyzed muscles,
which in the case of the orbicularis palpebrarum is of great
importance in preventing the eversion of the lower lid and the
overflow of the tears. As it is impossible during the first days
succeeding the paralysis to distinguish severe cases from those of
the middle form, it is best to begin the treatment of all cases in the
manner above described. The use of strychnia in rheumatic facial
paralysis, both internally and by hypodermic injection, may be
mentioned on account of the widespread preposession in its favor,
and to point out distinctly its utter futility.

Mechanical appliances and manipulation are used with advantage in

the treatment of facial paralysis to prevent the paralyzed muscles
about the mouth and cheek from being drawn out of place and over-
stretched by the action of the sound ones of the opposite side, thus
having their tonicity and nutrition impaired.

Contractions and rigidity of muscles receive little benefit from the use
of electricity, and must be treated by mechanical procedures, such
as stretching, massage, etc.

Neuromata.

The term neuromata was applied to all tumors involving the nerve-
trunks at a time when their histological differences had not been
studied and they were all supposed to be composed of nerve-tissue;
and even yet the name is conveniently retained, because, although
differing widely histologically, tumors situated upon the nerves have
a very similar clinical history.

Neuromas must be divided into true and false, the true consisting of
nerve-tissue, the false, or pseudo-neuromas, being composed of
many varieties, having this only in common, that they are seated
upon the nerves.

The true neuromas are again subdivided into those in which the
nerve-tissue composing them resembles exactly the fibres of the
peripheral nerves, showing with the microscope the double-
contoured white substance of Schwann surrounding an axis-cylinder,
and those in which the tumor is made up of fibres which Virchow has
shown to be non-medullated nerve-fibres—i.e. the axis-cylinder
without the white substance of Schwann. These two forms have
been distinguished by the names myelinic and non-myelinic. The
true neuromas are non-malignant, although showing the tendency to
recur after extirpation, are of slow growth, and as a rule do not
increase to a very great size. The best type of the myelinic neuromas
is found in the spherical or spindle-shaped enlargements at the cut
ends of nerves, particularly in the stumps of amputated limbs, where
they are found oftenest intimately connected with the cicatricial
tissue, though sometimes lying free. They consist of true medullated
fibres mixed with some fibrous tissue. The fibres composing them
are derived partly from splitting up and proliferation of the fibres of
the nerve itself, partly are of new formation, the appearances
strongly recalling the process of regeneration in nerves. Myelinic
neuromas consist of fibres and nuclei so closely resembling in
microscopic appearance the fibromas that they have hitherto been
confounded with them; and there is a difference among the highest
authorities as to the certainty of their diagnosis, and, in
consequence, of the frequency of their occurrence. The true
neuromas may include in their structure all of the fibres of the nerve-
trunk or only a portion of them (partial neuroma)—a fact of
importance in their symptomatology. Of the false neuromas, the
fibromas are by far the most frequently met with. They appear as
knots, more or less hard, upon the course of the nerve-trunk, which
they may involve completely or partially. They are often excessively
painful to the touch or spontaneously, most of the so-called tubercula
dolorosa belonging to the fibro-neuromas. Fibromas sometimes
occur along the trunk and branches of a nerve, forming a plexus of
knotted cords (plexiform neuroma). Fibro-sarcomas are not an
infrequent form of neuroma.

Myxomas often occur upon the peripheral nerves, and are frequently
multiple, their points of predilection being the larger trunks, as the
sciatic, ulnar, etc. They show their characteristic soft structure, and
are usually spindle-shape, assuming a rounder form as they attain a
large size. The various forms of sarcoma occasionally form tumors
upon the nerves, attacking generally the large trunks. Carcinomatous
tumors beginning upon the nerves sometimes occur, but as a rule
these growths involve the nerve by extension to it from adjacent
parts.

Syphilitic gummata have been found almost exclusively upon the

intracranial portion of the cranial nerves.

Gliomas appear to affect only the optic and acoustic nerves. Lepra
nervorum (lepra anæsthetica) produces usually a spindle-form
thickening upon the nerve-trunks, but sometimes there are more
distinct knots, which may be felt beneath the skin, bead-like, along
the course of the nerves of the extremities.

Like the true neuromas, the false neuromas, developing from the
neurilemma and perineurium, may involve the whole or only a part of
the fibres of a nerve, or the nerve-fibres may run at the side of the
tumor—different conditions, which may alter materially the effects
produced upon the nerve.

Neuromas, both false and true, may occur not only singly, but often
in large numbers, many hundreds having been counted upon an
individual. Sometimes they are numerous upon a single nerve-trunk
and its branches, and again they may appear scattered over nearly
all of the nerves of the body, even to the cauda equina and roots of
the nerves. According to Erb,9 isolated neuromas are more frequent
in females, while multiple neuromas are found almost exclusively in
men. Neuromas vary greatly in size, as we might expect from the
very great difference of their nature and structure; sometimes no
larger than a pea, they may attain the size of a child's head.
9 Ziemssen's Handbuch.

ETIOLOGY.—In cases of multiple neuromata it would seem as if there

was a constitutional condition or diathesis as the foundation of the
affection. This we may the more readily believe as there appears
good evidence to show that the tendency to the formation of these
nerve-tumors is sometimes hereditary, and some of them are
congenital.

Idiots and cretins have been observed to suffer in undue proportion

with multiple neuromas. We find a direct exciting cause of neuromas
in mechanical injuries of nerves, wounds, blows, pressure, etc. Thus,
as has been already seen, true neuromas occur in the divided ends
of the nerves after amputations or otherwise where a nerve-trunk
has been divided (cicatricial neuroma). As such neuromas are in
some degree the result of inflammation, it is probable that they may
sometimes be caused by chronic neuritis.

For a large number of neuromas no cause can be assigned, and we

must at present consider them as originating spontaneously.

SYMPTOMS.—The position and connections of neuromas being so

different, sometimes simply in contact with the nerve; sometimes
situated in the thickness of the nerve-trunk, the fibres being pressed
aside and spread out upon the surface of the tumor; sometimes
involving in their tissue a part or the whole of the nerve-fibres,—we
cannot but expect a very marked difference in their clinical history.
Not a few cases occur in which the presence of neuromas, even in
large numbers, gives rise to no symptoms during life, and their
existence has been revealed only upon a post-mortem examination.

The symptom most common to neuromas, and one to be expected

from their mechanical interference with the nerves, is neuralgic pain
—sometimes extreme, local or shooting along the course of the
nerves, stubborn, and hardly to be alleviated by remedies. It is
paroxysmal, notwithstanding the unvarying character of its cause, in
consonance with the tendency to periodical activity which prevails in
the nervous system. Sometimes the pain is increased notably by
atmospheric changes. The pain may sometimes be arrested by firm
pressure upon the nerve above the seat of the tumor. In some cases
pressure upon the neuroma, or even handling it, causes great pain.
The intensity of the pain does not depend upon the size of the tumor,
some of the smallest having earned the appropriate name of
tubercula dolorosa. The continued irritation of a neuroma sometimes
produces a condition of general nervous excitability, which shows
itself in hysterical and even in true epileptic convulsions.
Occasionally there are abnormal sensations (paræsthesiæ),
formication, numbness, etc., in the distribution of the nerve affected,
and when from pressure or histological changes the fibres are
destroyed anæsthesia results.

The interference with the conductivity of the motor fibres, which

occurs less frequently than alterations of sensation, shows itself in
cramps, tumors, paresis, and paralysis, according to its degree.

Neuromas may destroy life by the continued excessive pain, which

wears down the strength and depresses the vitality. Death may be
caused by their peculiar situation; as, for instance, upon the cauda
equina, where they produce paraplegia, paralysis of the sphincter
and bladder, and trophic changes.

The DIAGNOSIS of neuromas can only be made when they are

sufficiently superficial to be recognized by the touch, and along with
the symptoms above detailed the tumor is situated upon the known
course of a nerve, to which, moreover, its attachment allows a lateral
movement.

The only TREATMENT available for neuromas is extirpation, which must

be conducted with a view to sparing any fibres of the nerve not
involved in the tumor. Where it is necessary to divide the nerve in the
removal of the tumor, as small a portion as possible must be
excised, with the hope of a regeneration and reuniting of the cut
ends. The success of extirpation depends largely upon the nature of
the neuroma. The true neuromas, while they often show a strong
tendency to recur after removal, are benign and show no metastasis.
For the false neuromas the prognosis will be in accordance with their
benign or malignant character.
NEURALGIA.
 BY J. J. PUTNAM, M.D.

DEFINITION.—It is customary to describe as neuralgic those pains for

which no adequate cause can be assigned in any irritation of the
sensory nerves from outside, which recur paroxysmally, are
unattended by fever, and are distributed along the course of one or
more nerves or nerve-branches.

The general use of the term neuralgia further implies the common
belief that there is a disease or neurosis, not covered by any other
designation, of which these pains are the characteristic symptom. Of
the pathological anatomy of such a disease, however, nothing is
known; and if it could be shown for any given group of cases that the
symptoms which they present could be explained by referring them
to pathological conditions with which we are already familiar, these
cases would no longer properly be classified under the head of
neuralgia.

The attempt has frequently been made, and on good grounds, in

obedience to this reasoning, to cut down the list of the neuralgias,
strictly so called, and to account for many of the groups of symptoms
usually classified under that head by referring them to anæmia or
congestion of the sensory nerves, to neuritis, etc.

One of the best and most recent statements of this view is that of
Hallopeau,1 who, although he does not wholly deny the existence of
a neurosis which may manifest itself as neuralgia, goes so far as to
maintain that the gradual onset and decline and more or less
protracted course so common in the superficial neuralgias, such as
sciatica, suggest rather the phases of an inflammatory process than
the transitions of a functional neurotic outbreak, and that, in general
terms, a number of distinct affections are often included under the
name of neuralgia which are really of different origin, one from the
other, and resemble each other only superficially. This subject will be
discussed in the section on Pathology, and until then we shall, for
convenience' sake, treat of the various neuralgic attacks as if they
were modifications of one and the same disease.
1 Nouveau Dict. de Méd. et de Chir. pratiques, art. “Névalgies.”

GENERAL SYMPTOMATOLOGY.—The neuralgias may be conveniently

divided into—1, external or superficial; 2, visceral; 3, migraine and
the migrainoid headaches.

Superficial Neuralgia.

The most prominent symptom of a neuralgic attack of the superficial

nerves is of course the pain, and sometimes, from first to last, no
other sign of disease is present. In an acute attack the pain is usually
ushered in by a sense of discomfort, which the patient vainly tries to
shake off, or by a feeling of weight and pressure or of numbness and
prickling, or of itching. Sometimes, though far less often than in the
case of migraine, there are prodromal signs of a more general
character, such as a feeling of thirst2 or of mental depression or
drowsiness.
2 Spoken of by Mitchell's patient with neuralgia of the stump (see below).

A dart of pain may then be felt, which soon disappears, but again
returns, covering this time a wider area or occupying a new spot as
well as the old. The intensity, extension, and frequency of the
paroxysms then increase with greater or less rapidity, but, as a rule,
certain spots remain as foci of pain, which radiates from them in
various directions, principally up or down in the track of the nerve-
trunk mainly implicated. The pain rarely or never occupies the whole
course and region of distribution of a large nerve or plexus, but only
certain portions, which may be nearly isolated from one another.
In an acute attack the affected parts may at first look pale and feel
chilly, and later they frequently become congested and throb.
Mucous surfaces or glandular organs in the neighborhood often
secrete profusely, sometimes after passing through a preliminary
stage of dryness.

The skin often becomes acutely sensitive to the touch, even though
firm, deep pressure may relieve the suffering. Movement of the
painful parts, whether active or passive, is apt to increase the pain.
When the attack is at its height, the pain is apt to be felt over a larger
area than at an earlier or a later period, and may involve other
nerves than those first attacked. Thus, a brachial becomes a cervico-
brachial neuralgia or involves also the mammary or intercostal
nerves. A peculiarly close relationship exists between the neuralgias
of the trigeminal and of the occipital nerves. It is said that when the
attack is severe the corresponding nerves of the opposite side may
become the seat of pain. This is perhaps remotely analogous to the
complete transference of the pain from one side to the other which is
so characteristic of periodical neuralgic headaches, especially if they
last more than one day.

Some cutaneous neuralgias pass away after a few hours' or a night's

rest, after the manner of a migraine or a headache, and patients in
whom this takes place are, as a rule, constitutionally subject to
neuralgia or other neuroses. Toward the end of such an attack there
is often a copious secretion of pale, limpid urine. In a large class of
cases, on the other hand, the attack is of several days' or weeks', or
even months' or years', duration, with remissions or intermissions
and exacerbations, which may be either periodical or irregular.

The most marked periodicity of recurrence is seen with the

neuralgias of malarial origin, which may take on any one of the
typical forms of that disease.

These malarial neuralgias affect pre-eminently, though not

exclusively, the supraorbital branch of the fifth nerve; but it should
not be forgotten that there is also a typically periodical supraorbital
neuralgia of non-malarial origin, of which the writer has seen several
pronounced examples, the pain usually recurring regularly every
morning at eight or nine o'clock and passing away early in the
afternoon. The same periodicity is seen, though less often, in other
neuralgias. Thus, Trousseau3 speaks of neuralgic attacks from
cancer of the uterus in a young woman, which recurred daily at
exactly the same hour. Some of the traumatic neuralgias show the
same peculiarity to a marked degree.
3 Clin. Méd.

In many neuralgias, on the other hand, the exacerbations are worse

at night, like the pains of neuritis. In the intervals between the attacks
the pain may be wholly absent, or may persist, usually as a dull
aching.

After a neuralgia has lasted a few days—sometimes, indeed, from

the outset if the attack is severe—it is usually found that definite
spots of tenderness have made their appearance at certain limited
points on the course of the nerve. These are the famous points
douloureux which Valleix described with such minute accuracy,
believing them to be invariably present in true neuralgias. This is
certainly not strictly the case, though they are very common. They
are not necessarily coincident with the foci of spontaneous pain, as
Valleix supposed, but do correspond in general to the points at which
the affected nerve emerges from its bony canal or from deep
muscles and fascia, and to portions of its area of distribution in the
skin. The spinous process corresponding to an affected spinal nerve
may also become tender, but this is probably to be looked on, like
the same symptom in so-called spinal irritation, not as a sign of local
disease, but as due to a general reaction on the part of the nervous
system, and as a fact of a different order from the tenderness along
the nerve.

The termination of an acute neuralgic attack is usually gradual, like

its onset, although in some cases of headache, and in other
neuralgias to a less degree, there comes a moment when the patient
suddenly declares that he is free from pain.