My apologies for not getting back to you sooner and my regrets for the reason you are here . . . but you couldn't find a better place to be for comfort.
I'll comment on the EMG and then give you my opinions and impressions to your story. Before I do any of that, let me explain what a motor neuron is, what a sensory neuron is and what a nerve is and I will do it in as layman a way as I can.
A motor neuron is a type of nerve cell that resides both in the upper part of the brain, the lower part of the brain (called the brainstem) and the spinal cord. Those that are in the upper part of the brain are called upper motor neurons and those that are in the brainstem and spinal cord are called lower motor neurons. The lower motor neurons directly contact our muscles and therefore directly control our muscles. The upper motor neurons contact the lower motor neurons but do not contact the muscles directly. Therefore, the upper motor neurons control the lower motor neurons and thus indirectly control our muscles.
A sensory neuron is a type of nerve cell that allows us to sense things in our environment. Therefore, it allows us to feel touch, pressure, pain, heat, cold, etc.
A neuron (whether it is an upper or lower motor neuron or a sensory neuron) is made-up of a soma (kind of like the "head" of the cell) and from that soma are "stringy" projections called axons (kind of like "arms that stem from the "head"). These axons are used for communication. The axons of upper motor neurons communicate with the lower motor neurons and the axons of lower motor neurons communicate with our muscles. Sensory axons relay sensory information to our brain. A bunch of axons bunched together is what a nerve is. Think of a nerve as a rope and the axons as the individual fibers of the rope.
With ALS, the soma's of lower motor neurons and upper motor neurons are destroyed. If the soma's are destroyed, that will start to destroy the axons. That gives rise to the signs of symptoms of the disease. When lower motor neurons are destroyed (because the lower motor neurons are directly controlling our muscels) it causes muscle weakness, followed by muscle atrophy and fasciculations. Damage to the upper motor neurons can be detected by an EMG. When upper motor neurons are damaged, it causes brisk reflexes, pathological reflexes, spasticity (very stiff muscles) and muscle cramps. The reason is because upper motor neurons inhibit lower motor neurons a bit. Therefore, when the upper motor neurons are destroyed, that inhibition is lost and that results in muscles that are over-stimulated and reflexes that are over-active, too.
With ALS, the sensory neurons and nerves are unaffected.
Now for the EMG:
Under "Sensory Studies" and "Motor Studies":
This is the NCS part of the EMG. "mV" is the size of the electrical activity of nerves and "ms" and "m/s" are the speed at which that electrical activity travels along the nerves. A decrease in the size of the electrical activity indicates damage to the nerve itself and a decrease in the speed indicates damage to the insulation around the nerves. If the values are normal, then there is no detectable damage to a nerve and the insulation is intact.
A sensory study is measuring the above electrical activity in sensory nerves. If the sensory nerves are not damaged, then those readings should be normal. With ALS, all of those readings should also be normal, because ALS does not affect sensory neurons. The readings were indeed normal with your father. Having said that, there are a number of other conditions that can spare sensory nerves but still cause the types of signs and symptoms your father has because those conditions affect motor nerves..
A motor study is measuring the above electrical activity in motor nerves. Even though ALS affects motor neurons and thus motor nerves, the size of the electrical activity should be relatively unchanged in its early stages. As the disease progresses, the size of the electrical acitivity in motor nerves will start to become evident. The insulation should remain intact with ALS (although in later stages it will be destroyed), so the speed of the electrical activity should be normal with ALS. The motor study appears to be normal with your father.
The Electromyography part of the EMG study follows, which is what pointed his neuro towards ALS.
Some terminology before I begin. Fibrilation potentials (fibs) and positive sharp waves (psw's) are a measure of spontaneous, electrical activity in an individual muscle cell (individual muscle cells make-up entire muscles) . Muscle cells should not have this activity under normal conditions. If they do, it means they are actively losing contact with the axons that control them (i.e. the axons from the lower motor neurons). This is called active denervation. This is something seen with ALS but is also seen with many, many, many, many other conditions. An MUAP (i.e. a motor unit potential) is electrical activity in a group of muscle cells and there is a normal value for this. If it is longer in duration and/or bigger in size than normal, then it is a sign that reinnervation has taken place. Reinnervation means that muscle cells have first been denervated from their healthy axons (I explained that above) but then undamaged axons take their place and recontact the muscle cells. When this happens, it causes restructuring of muscle cells and a subsequent increase in the duration and/or size of the MUAP. This is seen with ALS but again, is also seen in many, many, many, many other conditions.
Your father has fibs and psw's in both his right and left deltoid muscles (i.e. shoulder muscles). His MUAP's are also longer in duration. Therefore he has active denervation and reinnervation in both of those muscles. His left and right FDIO muscles (muscles between his finger and thumb) show the same pattern. His right and left tibialis anterior and EDB muscles (muscles on the front of his shin) also show the same pattern.. His left and right gastrocnemius (calf muscle), left and right biceps and triceps (muscles of his upper arms), left and right EDC and brachioradialis (muscles of his forearm) only show reinnervation. It also says that he has signs of denervation in his genioglassus area (i.e. bulbar region), which is related to the tongue.
With ALS, active denervation and reinnervation will be seen in multiple muscles in multiple areas of the body. In fact, there are criteria that must be met before a definite ALS diagnosis is given. There must be three different areas of the body that are affected and it must be in multiple regions of those areas. It appears that your father has met those criteria. There must also be clinical signs of upper motor neuron damage (i.e. brisk reflexes, spasticity, etc.) seen. You have not made mention of any other those. The history must also be consistent with ALS. That is where the snag is. You say that he has had bouts of clinical weakness with subsequent improvement. That is not at all how ALS works. Once an area is weakened, there is no way to make improvements because the death of the motor neurons is permanent. Having said that, it is my guess that his neuro is thinking that something else was happening simultaneously with ALS and that's how the improvement was made.
Bottom line: it is not 100% definite that your father has ALS. Even if there is a tiny percent chance he doesn't have it, you shoud get a second opinion, which is what you are now doing. Please let us know how that goes and please let me know if there is anything I need to clarify.